Flash Pulmonary Edema in Patients with Chronic Kidney ... · Flash Pulmonary Edema Flash pulmonary edema can origi-Flash Pulmonary Edema in Patients with Chronic Kidney Disease and

NEPHROLOGY NURSING JOURNAL ■ January-February 2007 ■ Vol. 34, No. 1 15

Flash Pulmonary Edema in Patientswith Chronic Kidney Disease andEnd Stage Renal Disease

Carol M. Headley, DNSc, RN, CNN, isNephrology Advanced Practice Nurse at The VAMedical Center, Memphis, TN. She is ANNA’sNational Program chairperson and a member ofANNA’s Memphis Blues Chapter.

Barry M. Wall, MD, is Professor of Medicine atThe University of Tennessee Health Science Center,Memphis, TN, and Nephrology, Associate Chief atThe VA Medical Center, Memphis, TN.

Note: The authors reported no actual or potentialconflict of interest in relation to this continuingnursing education article.

Flash pulmonary edema andacute pulmonary edema areterms used to define the suddendevelopment of respiratory dis-

tress related to the rapid accumula-tion of fluid within the lung intersti-tium secondary to elevated cardiacfilling pressures (Little, & Braunwald,1997). For the purposes of this review,flash pulmonary edema will be theterm used. One of the first studies todescribe its occurrence linked itsdevelopment to individuals with pre-existing coronary artery disease andhypertension (Lee, Cabin, & Francis,1988). The connection between flashpulmonary edema and kidney diseasewas initially described in individualswith bilateral renal artery stenosis(Pickering et al., 1988). This associa-tion has been so well characterizedthat the recommendation has beenmade that anyone presenting withflash pulmonary edema be consid-ered for evaluation for renal arterystenosis (Missouris, Belli, &MacGregor, 2000).

The risk for flash pulmonaryedema in individuals with chronickidney disease (CKD), primarily endstage renal disease (ESRD), has beenunder emphasized in the literature.There are several possible explana-tions for the lack of reports describingan association between flash pul-monary edema and CKD, especiallyin patients with CKD receiving main-

tenance dialysis. The sudden onset ofpulmonary edema may be assumedto be from excessive interdialyticweight gain, inaccurate dry weightprescription, or weight scale malfunc-tions rather than from a cardiogenicorigin. Furthermore, treatment isoften readily available and imple-mented (ultrafiltration), thus the prob-lem is promptly treated.

The strong association betweencardiovascular disease and kidneydisease has been emphasized during

the past decade (Foley, Parfrey, &Samak, 1998). Kidney disease is nowknown to be an independent risk fac-tor for cardiovascular morbidity andmortality (Levey et al., 1998; Sarnaket al., 2003). This article will defineflash pulmonary edema and factorsfor its development, emphasizing therelationship between cardiovasculardisease and chronic kidney disease.Lastly, a case study of a patient onhemodialysis that developed flashpulmonary edema will be presented.

Flash pulmonary edema, also termed acute onset pulmonary edema, is characterized by thesudden onset of respiratory distress related to accumulation of fluid in the lung interstitiumover 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 pulmonaryedema. This article highlights the connection between cardiac pathologies found in chronickidney 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 withchronic kidney disease and ESRD.

Objectives1. Identify causes of flash pulmonary edema that may occur in conjunction

with chronic kidney disease and ESRD2. 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.

Continuing NursingEducation

Carol M. Headley Barry M. Wall

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 NursesCredentialing Center’s Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP00910.

The Nephrology Nursing Certification Commission (NNCC) requires 60 contact hours for eachrecertification period for all nephrology nurses. Forty-five of these 60 hours must be specific to nephrologynursing 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. 116

and interstitial fluid oncotic pressures,and the pressure differential acrossthe capillary wall). Normally, thealveolar bed within the lung serves toprotect the lung from fluid accumula-tion. Alveoli have very low perme-ability for fluid and protein. Any fluidfiltered into the alveoli is continuous-ly absorbed back into the interstitiumby the alveolar epithelial cells anddrained away from the pulmonaryinterstitium by lymphatic vessels(Gluecker et al., 1999).

Non-cardiogenic pulmonary edemaoccurs as a result of fluid accumula-tion in the alveoli resulting from adisruption in Starling’s forces sec-ondary to increased capillary perme-ability. The most common cause ofnon-cardiogenic pulmonary edema isacute lung injury (ALI) or acute res-piratory distress syndrome (ARDS)associated with increased pulmonarycapillary permeability. Most often,the concentration of protein withinthe pulmonary interstitium exceeds60% of the plasma protein value ascompared to less than 45% in cardio-genic pulmonary edema (Hanley &Welsh, 2004). Non-cardiogenic pul-monary edema is diagnosed whenthere is radiographic evidence ofalveolar fluid accumulation withoutan elevation in the pulmonary wedgepressure greater than 18 mmHg orevidence of congestive heart failure(CHF) on physical examination(Mason, Broaddus, Murray, & Nadel,2005).

Cardiogenic pulmonary edema isthe most common type of pul-monary edema and results from

increased left atrial filling pressure(Hanley & Welsh, 2004). In this typeof pulmonary edema, the rate offluid accumulation within the lungsis mainly dependent upon the func-tional capacity of the lymphatic sys-tem of the lungs to remove fluidfrom the interstitium and alveoli(Mason et al., 2005). As left atrialpressure rises, pulmonary capillarypressures increase resulting in pro-tein poor fluid (edema) being forcedinto the lung interstitium and alveoli.Consequently, there is a progressivedeterioration in alveolar gasexchange resulting in hypoxemiaand symptoms of respiratory dis-tress. Compensatory changes mayoccur in individuals with chronicallyelevated left atrial pressures and per-sistently elevated pulmonary capil-lary wedge pressures (greater than 18mmHg). In this circumstance, thelymphatic system of the lungsbecomes more efficient at removingfluid, thus reducing the likelihood fordevelopment of edema. It is the sud-den or acute elevations in left atrialpressures that are more likely toresult in acute pulmonary edema(Fraser, Müller, Colman, & Paré,1999; Little, & Braunwald, 1997).

It may be difficult to differentiatebetween flash pulmonary edema andnon-cardiogenic pulmonary edemasince the presenting symptoms areoften the same (Hanley & Welsh,2004). Symptoms typically consist ofdyspnea, tachypnea, and cough withpossible expectoration of frothyedema fluid. The patient history anddetermination of the factors that ledto the development of the pul-monary edema becomes a priorityfor diagnosis. Non-cardiogenic pul-monary edema is less common andis primarily seen in individuals thathave had recent pneumonia, sepsis,tumor, pulmonary fibrosis, traumawith multiple blood transfusions, fol-lowing lung transplantation or resul-tant from aspiration of gastric con-tents.

Flash Pulmonary EdemaFlash pulmonary edema can origi-

Flash Pulmonary Edema in Patients with Chronic Kidney Disease and End Stage Renal Disease

Pathogenesis of PulmonaryEdema

Edema has been described asincreased volume within severalspaces of the body including theblood vessels (increase in blood vol-ume), the lungs (pulmonary intersti-tium and alveoli), the trunk and lowerextremities (peripheral edema), aswell as cavities within the abdomenand lungs (i.e., pleural effusions andascites). Peripheral edema is most evi-dent in the lower extremities becauseof the effect of gravity. The occur-rence of peripheral edema in patientswith CKD may be attributed to eitherheavy proteinuria (over 3.5 gramstermed nephrotic syndrome) oradvanced deterioration in kidneyfunction (Bickley, Hoekelman, &Bates, 1999). Pulmonary edemaresults from fluid accumulation in thelungs at a higher rate than can beremoved. The type of abnormalityexpressed in the Starling equation(Figure 1) differentiates the type ofpulmonary edema.. It can predict thenet flow of fluid across a membranebased upon permeability, surfacearea, and hydraulic pressures (Hanley& Welsh, 2004).

Pulmonary edema has been classi-fied into two categories dependentupon the underlying cause: cardio-genic and non-cardiogenic (Hanley &Welsh, 2004). Starling forces identi-fied in the equation affect the fluidbalance between the interstitium andthe vascular bed within the lungs(capillary permeability, capillary sur-face area, capillary and interstitialfluid hydraulic pressures, capillary

Q = K[(Pmv-Ppmv)-(mv-pmv)]

Q – net transvascular flow of fluidK – membrane permeabilityPmv – hydraulic pressure in the microvesselsPpmv – hydrostatic pressure in the perimicrovascular interstitiumππmv – plasma protein osmotic pressure in the circulationππpmv – protein osmotic pressure in the perimicrovascular interstitium

Figure 1Starling Equation

Note: From Staub, N.C.(1974). Pulmonary edema. Physiology Review, 54(3), page 680.


nervous systems becomes maladap-tive by contributing to cardiacmyocyte apoptosis (programmed celldeath), hypertrophy, and focalmyocardial necrosis ( Jackson et al.,2000).

Diastolic dysfunction, defined as adisorder of myocardial relaxationresulting in impaired ventricular fill-ing, may also result in the syndromeof congestive heart failure. Diastolicheart failure is diagnosed when ele-vated filling pressures are necessaryto achieve normal ventricular filling(Grossman 2000). Recent epidemio-

logic data has determined that 40% -50% of patients presenting with con-gestive heart failure have diastolicdysfunction as the predominant etiol-ogy. The diagnosis of diastolic heartfailure is made based upon the exis-tence of heart failure in patients withnormal systolic function (left ventricu-lar ejection fraction of 50% or greater)and no evidence of valvular or peri-cardial disease (Vasan, Benjamin, &Levy 1995). Some individuals willhave evidence of both systolic anddiastolic heart failure contributing todevelopment of flash pulmonary

nate from cardiogenic (i.e., cardiacdysfunction) and non-cardiogreniccauses (i.e., neurogenic pulmonaryedema) and occurs suddenly over aperiod of minutes to hours (Lee, et al.,1988). The syndrome of congestiveheart failure is the most common eti-ology for the development of flashpulmonary edema. Traditionally, thediagnosis of congestive heart failurehas been attributed to the presence ofmyocardial systolic dysfunction,defined as a disorder of myocardialcontractility leading to a reduced ejec-tion fraction. Chronic systolic dys-function results in a systemic process,not solely confined to the heart(Torre-Amione, 2005). Congestiveheart failure is a multisystem disorderaffecting the heart, skeletal muscle,kidneys, and nervous system pat-terned by a complex neurohormonalprocess. Figure 2 depicts a simplifiedversion of the process. Neuro-hormonal activation is key to the pro-gressive nature of chronic heart fail-ure whereas flash pulmonary edemaoccurs quickly and is primarilydependent upon a pre-existing condi-tion (i.e., diastolic dysfunction) cou-pled with an acute stressor (i.e., rise inblood pressure).

Chronic heart failure has been achallenge to treat because of its com-plexity and its insidious character.Initially, neurohormonal changes pre-sent in chronic heart failure are com-pensatory and temporarily improvecardiac 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-vides improved inotropic support toincrease cardiac output. Stimulationof the renin-angiotensin-aldosteronesystem (RAAS) causes release ofrenin, plasma angiotensin II, andaldosterone. Angiotensin II causesvasoconstriction of the efferent arteri-oles and the systemic circulation andincreased adrenal secretion of aldos-terone that results in sodium andwater retention by the kidneys( Jackson, Gibbs, Davies, & Lip,2000). However, long-term stimula-tion of the RAAS and sympathetic

Figure 2Neurohormonal Responses in Heart Failure

Impairmentin Left

Ventricular Function

Reductionin Cardiac

Output

SympatheticNervousSystem

IncreasedOxygen

Demands

RAASVasoconstriction

andSalt & Water

Retention

NatriureticPeptides

Natriuresis &Vasodilatation.

ChronicNeurohormonal

ActivationIncreasedPreload &Afterload

Cardiac Remodeling Further Heart

FailureMyocyte Apoptosis,Hypertrophy, Focal

Myocardial Necrosis


edema. However, diastolic heart fail-ure occurs more frequently in patientswith preserved systolic function, thusit has been attributed primarily to thedisorder of diastolic dysfunction(Gandhi et al., 2001).

Although diastole involves theprocess of cardiac relaxation, activeenergy requiring processes occur dur-ing this phase. The changes in cardiacpressure that occur during diastoleare the result of isovolumetric relax-ation from the time of the aortic valveclosure to mitral valve opening; earlyrapid filling after mitral valve open-ing; and low blood flow during mid-diastole; and lastly late filling (highblood flow) from atrial contraction. Indiastolic heart failure, the left ventri-cle is stiff (reduced elastic recoil) withimpaired 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 strongassociation between hypertensionand development of diastolic heartfailure, as well as a strong associationwith development of flash pulmonaryedema. One study described the pres-ence of systolic hypertension (systolicarterial blood pressure greater than160 mmHg) in 85% of patients pre-senting to hospital emergency roomswith flash pulmonary edema(Kramer, Kirkman, Kitzman, & Little,2000). Studies that performedDoppler echocardiography after theacute episode found preserved sys-tolic function (left ventricular ejectionfraction of 50% or greater) in themajority of patients presenting withflash pulmonary edema. Even thoughsystolic function was assessed as nor-mal, the evaluation was obtained aftertreatment of the hypertensive episodeand resolution of the pulmonaryedema, thus the presence of transientsystolic dysfunction as a precipitatingcause could not be excluded(Mansoor, Shah, & Scoble, 2001). Theprimary cause for flash pulmonaryedema, systolic versus diastolic heartfailure, was addressed in a study thatexamined patients with two-dimen-sional transthoracic echocardiogra-

phy using color Doppler imaging dur-ing the acute phase of pulmonaryedema with a follow up exam per-formed 2-3 days later. The left ven-tricular ejection fraction during theacute episode was similar to the mea-surement obtained 2- 3 days after pre-sentation (N = 30). Thus, a normalleft ventricular ejection fraction in apatient with co-existing hypertensionand flash pulmonary edema suggeststhat the pulmonary edema is due todiastolic dysfunction. Transient sys-tolic dysfunction and severe mitralregurgitation were found to be infre-quent causes for development of flashpulmonary edema (Gandhi et al.,2001)

Other clinical conditions that havebeen identified as contributing to thedevelopment of flash pulmonaryedema include: a) myocardialischemia, b) acute aortic insufficiency,c) acute mitral regurgitation, d) mitralstenosis, and e) renovascular hyper-tension (Walker, Walker, & Nielsen,2001), but this paper will primarilyfocus on diastolic heart failure as itrelates to development of flash pul-monary edema because diastolicheart failure has received less atten-tion and yet is believed to be highlyprevalent.

Cardiac DiseaseFlash pulmonary edema occurs as

a consequence of a disruption in thenormal pressure-volume relationshipduring the cardiac cycle. Ischemicheart disease/coronary artery diseasehas been linked with development offlash pulmonary edema. Acutemyocardial ischemia has been shownto cause systolic and diastolic dys-function. Cocaine abuse has beenassociated with development of flashpulmonary edema for multiple rea-sons including its precipitation ofmyocardial ischemia (coronary arteryvasoconstriction), acute rise in bloodpressure (peripheral vasoconstric-tion), and development of systolic aswell as diastolic dysfunction (Lange &Hillis, 2001).

The existence of coronary arterydisease can cause intermittent

episodes of diastolic dysfunction andsystolic dysfunction (Mansoor et al.,2001). Systolic dysfunction occurswhen there is less forward movementof blood from the heart prompting anincrease in diastolic volume and dias-tolic pressure precipitating pul-monary vascular congestion leadingto pulmonary edema. In diastolicheart failure, the myocardium is lesscompliant, such that the left ventricleis unable to accept an adequate vol-ume of blood from the venous systemand to fill at normal low pressures(Beattie, 2000). The net result is a risein diastolic pressures in order to pro-vide adequate ventricular filling.Heart failure resulting from diastolicdysfunction occurs when elevated fill-ing pressures are necessary to achievenormal ventricular filling (Grossman,2000). The increased resistance todiastolic ventricular filling is mostcommonly due to myocardial abnor-malities (myocardial hypertrophy,fibrosis, ischemia, or cardiomyopa-thy), and less commonly to mechani-cal abnormalities like mitral stenosisor constrictive pericarditis (Hanley &Welsh, 2004).

Hypertension is frequently pre-sent in patients presenting with flashpulmonary edema. Chronic hyper-tension that is poorly controlled canresult in development of systolic anddiastolic dysfunction that may predis-pose patients to the development offlash pulmonary edema (Mansoor etal., 2001). Even labile elevations inblood pressures of patients with bilat-eral renal artery stenosis have beenshown to be associated with anincreased risk for development offlash pulmonary edema (Bloch, Trost,Pickering, & Sos, 1999). As noted byVasan & Levy (1996) long standinghypertension is a primary predeces-sor to development of left ventricularhypertrophy (LVH). Hypertensionleads to remodeling and augmenta-tion of the left ventricular mass thatcan result in diastolic dysfunction,systolic dysfunction, or both.However, it is important to realizethat not everyone with LVH willdevelop heart failure. Athletes some-times acquire what is called physio-



logic hypertrophy of the left ventricleand maintain near or near-normalexercise tolerance. Therefore, LVHby itself does not constitute cardiacdysfunction (Lorell & Carabello,2000).

Renal Artery Stenosis and FlashPulmonary Edema

Renal artery stenosis (RAS) maybe identified in individuals withapparent normal kidney function aswell as those with a diagnosis of acuteor chronic kidney disease (Missouris,Belli, & MacGregor, 2000). Renalartery stenosis (narrowing of the renalartery) is most often a result of ather-osclerosis. Fibromuscular dysplasia, isa rare idiopathic condition in whichthere is an increase in the number ofcells in the renal artery cell wallresulting in arterial narrowing.Atherosclerotic lesions result from thedeposition of plaque within the renalartery and are most often seen in indi-viduals over the age of 55, whilefibromuscular dysplasia is usuallyseen in young women. Women withfibromuscular dysplasia associatedRAS almost invariably have hyper-tension. Lesions associated with fibro-muscular dysplasia tend to show amuch more favorable response topercutaneous transluminal angioplas-ty (PTA), stent or surgery than athero-sclerotic lesions (Olin, 2004).

The most common type of RASinvolves atherosclerotic deposition inthe artery lumen that disrupts bloodflow to the kidney parenchyma caus-ing ischemia. The kidney responds bysecreting renin into the bloodstream,leading to the production ofangiotensin II, which is both a potentvasoconstrictor and a major stimulusfor adrenal secretion of aldosterone(Safian & Textor, 2001). Hypertensionresulting from activation of the RAASis referred to as renovascular hyper-tension. Mild to moderate hyperten-sion is not commonly associated withRAS; however, malignant and drugresistant hypertension carries a highdegree of suspicion for RAS, havingbeen diagnosed in up to a third ofpatients having difficult to control or

malignant hypertension (Harding etal., 1992). Renovascular hypertensionrelated to bilateral renal artery steno-sis is strongly associated with thedevelopment of flash pulmonaryedema. The combination of hyper-tension and volume retention, occur-ring as a consequence of alteredintrarenal hemodynamics and aldos-terone-mediated salt and water reten-tion are the major contributing factosto the development of flash pul-monary edema with bilateral renalartery stenosis. In contrast pulmonaryedema is relatively uncommon withunilateral renal artery stenosis(Basaria & Fred, 2002; Jaff, 2001).Unilateral renal artery stenosis leadsto renin dependent hypertension, butnot to volume expansion, since thenon-affected kidney undergoes apressure natriuresis/diuresis, whichprevents volume expansion makingpulmonary edema less likely to occur(Missouris et al., 2000).

Flash Pulmonary Edema andKidney Disease

Many of the precipitating factorsassociated with development of flashpulmonary edema are frequently pre-sent in patients with advanced stagesof CKD (Table 1). Cardiovascular dis-ease and CKD are strongly linked.Recent findings indicate that patientswith CKD are in the highest riskgroup for cardiovascular disease andthat patients with CKD are more like-ly to die of cardiovascular diseasethan ESRD (Levin, 2003).

Systolic and diastolic heart failure

has been associated with the develop-ment of flash pulmonary edema(Ware & Matthay, 2005). This discus-sion will primarily highlight thepathology of diastolic heart failure. Arelationship between the risk for dias-tolic heart failure in the presence ofkidney disease can be established byexamining the contributing factorsthat precede there development(Figure 3). Diastolic heart failure canbe caused by ischemia, left ventricu-lar hypertrophy (LVH), increased fill-ing pressures related to chronicallyelevated blood pressures, infiltrativecardiomyopathies, ischemic heart dis-ease, pericarditis, the normal agingprocesses, chemotherapy and geneticanomalies (Beattie, 2000; Kramer etal., 2000; Zile & Simsic, 2000). In thegeneral population, 50% of peopleover the age of 70 with a diagnosis ofcongestive heart failure will have pre-served systolic function and classifiedas having diastolic heart failure. Forthose 10 years younger (60 years ofage) with congestive heart failuresymptoms, only 15% will have dias-tolic heart failure. Age also con-tributes to mortality risk. Overall,prognosis is better for diastolic heartfailure (average mortality rate 5 % -8%) than for systolic heart failure(average mortality rate 10% - 15%),but diastolic heart failure in patientsover 70 years has a 50% 5-year mor-tality rate (Zile & Simsic, 2000). Thesechanges are similar to disease report-ed in the elderly, but they occur 15-20years earlier in kidney disease(Tozawa, Iseki, Iseki, & Takishita,2002; Churchill et al., 1992). Systolic

Table 1Prevalence 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 dialysispatient – 63 years

USRDS, 2005

Ischemic heart disease 35% - CKD40% - Beginning dialysis

Levin, 2003

Heart failure 37% Foley et al., 1994


and diastolic heart failure are highlyprevalent in patients with advancedCKD (Foley et al., 1994).

Increasing emphasis has beenplaced on the need to control bloodpressures in all stages of CKD. Sincehypertension is both a cause and acomplication of CKD, prevalencerates are high. Elevated blood pres-sure is a primary contributing factorto development of LVH and heartfailure (both systolic and diastolic).Lucas and colleagues (2003) foundthat systolic hypertension andincreased pulse pressures are com-mon at the time of dialysis initiation.All cause mortality was significantlyhigher, 14.1 deaths per 100 patient-years for patients with uncontrolledhypertension (BP greater than 140/90mmHg) compared to those that werenormotensive, 7.9 deaths per 100patient years (RR = 1.79, P = 0.01,95% CI = 1.15–2.8.). Blood pressurecontrol remains poor even afterbeginning renal replacement therapy.Reports indicate that blood pressurecontrol in patients receiving dialysis islow with 40% – 90% having bloodpressures higher than the NationalKidney Foundations K-DOQI rec-ommended goal of 140/90 pre-dialy-sis (Chalmers et al., 1999; Dhakal,Sloand, & Schiff, 2000; Salem, 1995).

Coronary artery disease has alsobeen recognized as a contributing fac-tor to development of flash pul-monary edema. Chronically elevatedblood pressure results in stiff arteriesthat have diffuse arteriosclerosis.Murphy (2003) reports a coronaryartery disease prevalence rate of 40%in patients beginning dialysis, 22%have stable angina and 8% have his-torical documentation of a previousmyocardial infarction.

The diagnosis of flash pulmonaryedema is made using a compilation ofclinical findings (Mansoor, et al.,2001). Initial evaluation shouldinclude a chest x-ray and Dopplerechocardiogram. Chest radiographscharacteristically demonstrate enlarge-ment of the peribronchovascularspaces, prominent septal lines as wellas acinar areas of increased opacitythat coalesce into frank consolidations


Decreased Glomerular

Filtration Rate

IncreasedExtracellularFluid Volume

Hypertension

CardiacRemodeling:

LVH

DiastolicDysfunction

Increased CardiacFilling Pressures

Flash PulmonaryEdema

Acute Rise in Blood Pressure

Figure 3Pathogenesis of Diastolic Heart Failure in CKD


invasive and can offer further supportin determining the existence of dias-tolic heart failure, especially whenthere is isolated maladaptive relax-ation of the ventricles.

If the Doppler echocardiogram isnon-conclusive or technically inade-quate due to a poor acoustic window,as often occurs in patients with anabnormal body habitus, then a multi-ple-gated acquisition (MUGA) scanotherwise known as a cardiac bloodpool scan may be required. This scanuses a radioactive isotope to evaluateventricular function and detect abnor-malities in the heart wall (Logeart etal., 2002). The MUGA is more accu-rate at calculating ejection fraction,but less efficient at identifying valve

morphology. The radio isotope (tech-netium) is injected into a vein andabsorbed immediately by healthy tis-sue. A gamma scintillation cameradetects the gamma rays emitted bythe radio isotope. If the patient’s heartis normal, the technetium will bereadily and evenly distributed in thecardiac images. An uneven distribu-tion of technetium in the heart maybe indicative of coronary artery dis-ease, cardiomyopathy, or bloodshunting within the heart. Use of thegamma scintillation camera exposesthe patient to about the same amountof radiation as a chest x-ray(Youngerman-Cole, 2005).

Even though rarely done, the goldstandard for the diagnosis of diastolic

(Ware & Matthay, 2005). It is oftendifficult to differentiate between sys-tolic and diastolic heart failure basedupon patient history, physical exam,chest radiograph, and EKG. Dopplerechocardiography is the most com-monly utilized technique to assessboth systolic and diastolic ventricularfunction. Diastolic function involvesboth active and passive components.The active phase involves energydependent relaxation while the pas-sive phase predominantly reflects theviscoelastic properties of the heart tis-sue.

Doppler echocardiography assess-es both of these phases by examiningpressure changes during transmitralflow (Figure 4) in diastole. Early dias-tolic flow occurs when the mitralvalve initially opens at the onset ofdiastole. The E wave determined byDoppler echocardiography serves asan index of left ventricular relaxation,compliance, and atrial pressure. Earlypassive ventricular filling is followedby the ventricular filling produced byatrial contraction (A wave). Deceler-ation time (DT) is a measurement ofthe time it takes for passive filling.Deceleration time will shorten whenthere is a decrease in left ventricularcompliance however decelerationtimes are also affected by otherpathologies that increase the left atrialpressure and shorten DT. DT valuesover 240 ms indicate impaired relax-ation, and under 150 ms indicate arestrictive pattern (Gilbert, Connelly,Kelly, Pollock, & Krum, 2006).Interpretation of E:A ratios becomesmore difficult when there are com-bined pathologies of impaired relax-ation and restriction, then both leftatrial and ventricular pressuresincrease leading to an increase in themagnitude of the E wave resulting ina normal E:A ratio (pseudonormalpattern) which can be unmasked bymaneuvers that alter cardiac preloadsuch as the Valsalva maneuver oradministration of nitroprusside(Angeja & Grossman, 2003). Eventhough there are problems with inter-pretation of E:A ratios, transmitralinflow patterns obtained withDoppler echocardiography are non-

Normal E: A Ratio and Deceleration Time

Deceleration Time

Restrictive E:A Ratio and Deceleration Time

Deceleration Time

Normal: 0.75 greater than E:A greater than 0.75, but less than 1.5 with DT 200± 32 msMild Diastolic Dysfunction: E:A greater than or equal to 0.75 with DT greaterthan or equal to 230 msModerate Diastolic Dysfunction ("Pseudonormal"): E:A greater than 0.75 butless than 1.5 with DT greater than 140 msSevere 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 andPrimary care perspective. Journal of the American Board of Family Practitioners,18(3), 189-198.

Figure 4Transmitral Pressures used in Diagnosis of Diastolic Dysfunction

E – Early passiveventricular filling

A – Ventricular filling produced byatrial contraction

DT

E – Early passiveventricular filling

A – Ventricular filling produced byatrial contractionD

T



heart failure continues to be cardiaccatheterization allowing direct mea-surement of volumes and pressures,but at significantly higher cost andrisk (Gutierrex & Blanchard, 2004). Itis usually not necessary to determinethe etiology for the heart failure sinceDoppler echocardiogram or MUGAusually provide adequate diagnosticcriteria. Pulmonary artery catheteriza-tion can also be done and has anadverse event rate of 4.5% - 9.5%, butit is much more precise in definingthe presence of diastolic heart failurethan MUGA or Doppler echocardio-gram alone. If the pulmonary arteryocclusion pressure is greater than 18mm Hg then cardiogenic pulmonaryedema exists (Harvey et al., 2005).

Laboratory testing in flash pul-monary edema typically may includemeasurement of plasma levels of tro-ponins and brain natriuretic peptide(BNP). Troponin I elevation in thepresence of kidney failure hasdemonstrated high prognostic valuefor acute coronary syndrome(myocardial ischemia). Troponin Televation has not been recommendedfor detecting acute myocardialischemia, but has been associatedwith increased mortality risk (Freda,Tang, Van Lente, Peacock, & Francis,2002). In a recent study of 258hemodialysis patients, elevations inTroponin 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 ofTroponin I (trend) may be required tomake a definitive diagnosis of acutecoronary syndrome since 1% -6%have been shown to have elevationswithout symptoms (Freda et al.,2002).

Elevations in brain natriuretic pep-tide (BNP) have been routinely usedin the diagnosis of heart failure. Whenthe ventricular wall stretches or thereis increased ventricular pressure, BNPis secreted. A recent consensus panelconcluded that BNP levels below 100pg/mL indicate that heart failure isunlikely (negative predictive value,greater than 90%); while a BNP levelgreater than 500 pg/ml indicates thatheart failure is likely (positive predic-

tive value, greater than 90%) (Silver etal., 2004). Intermediate levels of BNP,between 100 and 500 pg /mL had lessdiagnostic discrimination. BNP levelsmay be elevated in critically illpatients, even in the absence of heartfailure; however, BNP levels lessthan100 pg/ml continue to be usefulin excluding heart failure in thesepatients. BNP levels are also elevatedin patients with chronic kidney dis-ease, such that a cut off level below200 pg/mL has been suggested toexclude heart failure when the esti-mated glomerular filtration rate isbelow 60 mL per minute. Chronic ele-vations in BNP may also be a hall-mark of patients with or at risk fordiastolic heart failure among subjectswith preserved systolic function, inde-pendent of the degree of left ventricu-lar hypertrophy (Yamaguchi et al.,2004).

Symptoms of Flash PulmonaryEdema

Complaints of severe cough anddyspnea are usually the primarysymptoms on presentation of flashpulmonary edema with or withoutchest discomfort. Common findingson physical examination include:

• Tachypnea – with use of acces-sory muscles of breathing.

• Lung fields – auscultation ofcrackles in bases and scatteredthroughout the lung fields,rales or even decreased breathsounds.

• Cardiac exam – possible pres-ence of an S3 indicating anincrease in left ventricular enddiastolic volume or an S4 gal-lop coinciding with an increasein left atrial pressure, and anew or changed murmur.

• Jugular venous distension indi-cating increased filling pres-sures.

• Systolic Blood pressure – maybe markedly elevated. Hypo-tension suggests left ventricularsystolic dysfunction andimpending cardiogenic shock.

• Peripheral edema – usuallywithout signs of edema, if pre-

sent, then associated with long-standing volume expansion(Mason, Broaddus, Murray, &Nadel, 2005).

Flash Pulmonary Edema: A CasePresentation

A 54-year-old male presented tothe dialysis unit of an acute care hos-pital due to inadvertent dislodgementof his tunneled venous catheter. Hehad 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 havethis catheter removed and a newcatheter placed. He had undergonehemodialysis 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 tothe unit without difficulty. His bloodpressure was noticeably elevated andhe reported holding his antihyperten-sives that day in anticipation ofundergoing hemodialysis. Holdinghis antihypertensives on the day ofdialysis was a common practice. Achest radiograph was obtained priorto sending the patient to intervention-al radiology to evaluate for any evi-dence of volume expansion since hewould most likely miss his dialysistreatment that day (see Figure 5).

Physical examination on presenta-tion:

• Temperature: 97.8º F;• Weight: 71 Kg (less than 2 kg

above present dry weight esti-mate);

• Blood pressure: 165/116 HR89 (sitting); blood pressure151/88 HR 86 (standing);

• No evidence of jugular venousdistension;

• Cardiovascular exam: Regularrhythm, rate 89/minute, I/VIsystolic 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


clear to auscultation; and• No peripheral edema present. Past medical history was signifi-

cant for:• Coronary artery disease and

myocardial infarction – withcoronary 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 approximateejection fraction of 29%;

• Left ventricular diastolic dys-function;

• Mild eccentric left ventricularhypertrophy;

• Trace tricuspid regurgitation;and

• No pericardial effusion. The patient returned from the

interventional radiology departmentfollowing catheter removal and place-ment of a new cuffed hemodialysiscatheter on a stretcher. He was notedto be in acute respiratory distress withthe head of the stretcher at 90º.

The following findings were notedupon 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- tachy-

cardia, II/VI systolic murmur,loud S2, positive galloprhythm , no pericardial rub;

• Lungs - decreased breath soundsin lung bases;

• No peripheral edema noted;• 12 Lead EKG – Sinus tachy-

cardia with rate 127/minute,occasional premature ventricu-lar complexes, left atrialenlargement, left ventricularhypertrophy and non-specificST segment changes;

• Portable chest x-ray demon-strated a new dialysis catheterin place in the left internal

jugular vein with the tip in thesuperior vena cava. The previ-ously placed catheter had beenremoved. There was diffusebilateral pulmonary interstitialedema (see Figure 6);

• Serial Troponin I: 0.0 – 1.0ng/mL over 24 hours (Range:0 – 0.6 – no cardiac damage,0.7 – 1.5 – non-diagnostic,greater than 1.5 Evidence of amyocardial 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/dLThe 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.

Figure 5Standing Chest Radiograph AP Prior to

Undergoing Catheter ReplacementFigure 6

Portable Chest PA Radiograph 5 Hours Later


Hemodialysis was initiated withultrafiltration of 3.5 liters over a 4-hour period. The patient’s blood pres-sure improved, and he did not requireendotrachial intubation. The oxygenby non-rebreather facemask wasslowly weaned during dialysis to anasal cannula oxygen by the end ofthe dialysis treatment. He was admit-ted for observation and serial tro-ponins to rule out myocardial infarc-tion, all of which were negative. Hereturned home after 24 hours withinstructions to take his antihyperten-sive medications the night before dial-ysis to avoid the surge in blood pres-sure the morning prior to hishemodialysis treatments.

Nursing ImplicationsPulmonary edema is a common

complication of patients with ESRD(Evans, Reddan, & Szczech, 2004;Shapiro, Deshetler, & Stockard,1994). Fluid and salt abuse has beenreported to be the most commoncause of pulmonary edema in patientsreceiving renal replacement therapy.How does one differentiate betweenpulmonary edema that is associatedwith excessive fluid intake and car-diogenic mediated flash (acute) pul-monary edema? Pulmonary edemathat occurs without significant interdi-alytic weight gain or evidence ofperipheral edema on physical exami-nation, particularly in association withan elevation in blood pressure,strongly supports the diagnosis offlash pulmonary edema.

A history of ischemic heart dis-ease, poorly controlled hypertension,and identification of left ventricularhypertrophy by Doppler echocardio-graphy may signify an increased riskfor development of flash pulmonaryedema. Anemia and hypertensionhave been primarily associated withthe development of left ventricularhypertrophy and are found in themajority of patients beginning dialy-sis. Poorly controlled hypertension inthe presence of a remodeled heart(i.e., LVH) may result in diastolic dys-function which predisposes to thedevelopment of pulmonary edema

during episodes of volume expansion.The routine practice of holding anti-hypertensives prior to undergoinghemodialysis in certain circumstancesmay need to be reconsidered. Thepractice of holding antihypertensivesis to avoid low blood pressures at theend of dialysis following volumeremoval (Coomer, Schulman, Breyer,& Shyr 1997). Blood pressures tend tonormalize with the removal ofintravascular volume during the ultra-filtration process. It may be better toreduce rather than hold antihyperten-sives prior to dialysis to avoid suchextremes in blood pressure (Sulkova& Valek, 1988).

The immediate treatment ofpatients with flash pulmonary edemais essentially the same as with anyother type of pulmonary edema.Initial assessment should includemonitoring of hemodynamic parame-ters and pulse oxymetry or arterialblood gases. Patients should be givenoxygen. This oxygen support shouldbe 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 than200) endotrachial intubation may berequired (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 withultrafiltration if the patient hasalready been receiving dialysis ismost beneficial.

Medications commonly used inthe treatment of flash pulmonaryedema include a) nitroglycerin, b)furosemide, and c) morphine sulfate.Nitroglycerin is a potent vasodilatingdrug which increases cardiac outputwhile decreasing preload and after-load. Nitroglycerin reduces pul-monary edema mainly throughvenous dilatation. Patients receivingdialysis who are oliguric or anuricmay have a mild venodilatoryresponse to furosemide, but will nothave an effective diuresis. The benefitof morphine in treatment of pul-monary edema has remained contro-versial. Morphine will reduce blood

pressure and pulmonary edemathrough venous dilatation, but mor-phine may also cause respiratorydepression (Beattie, 2000). Loweringthe blood pressure is a priority withseverely elevated blood pressures.Labetalol is an effective antihyperten-sive to use in hypertensive crisis sinceit can be given intravenously withoutrenal adjustment (NHLBI, 2003). Itcan be given as a slow intravenouspush starting at 20 mg over 2 min-utes: additional 2 mg dosages can begiven every minute up to 300 mgmaximum dose to obtain a gradualreduction in blood pressure (NKF,2005). Lowering of the blood pres-sure reduces cardiac filling pressuresand allows cardiac output to improve,thus reducing fluid accumulation inthe lungs. Additionally slowing of theheart rate will improve diastolic fill-ing, thus improving stroke volumeand cardiac output.

Treatment of flash pulmonaryedema is aimed at resolving theimmediate threat of respiratory dis-tress and hypoxemia and eliminat-ing/treating the underlying cause (i.e.,hypertensive crisis). Nurses assesspatients’ blood pressures pre-dialysisand post-dialysis, thus they are thefirst to note changes that may placethat patient at risk. If blood pressuresare assessed as above the recom-mended pre-dialysis reading of140/90, then changes in the treatmentregimen can be instituted. It may benecessary to reduce the estimated dryweight to achieve a normalized pre-dialysis pressure or additional antihy-pertensives may be required. Whenhemodialysis is postponed or can-celed, then nurses need to remindpatients to resume their antihyperten-sives in order to avoid blood pressureextremes and risk of flash pulmonaryedema.

ConclusionPatients with CKD are at risk for

developing flash pulmonary edema.Cardiovascular disease is highlyprevalent in the kidney disease popu-lation. Diastolic heart failure is oftenunsuspected without clinical suspi-



cion since the presentation is similarto that seen with systolic heart failure.The prevalence of LVH at the timepatients begin dialysis increases thelikelihood of patients developing bothsystolic and diastolic dysfunctionwhich can lead to development offlash pulmonary edema. TheNational Kidney Foundation K-DOQI guidelines for cardiovasculardisease recommends that echocardio-grams be performed on all patients atthe initiation of dialysis and againafter achievement of prescribed dryweight and at 3 year intervals there-after (NKF, 2005). Nurses shouldacknowledge and recommend treat-ment of blood pressures that areassessed to be elevated beyond thecurrent pre-dialysis blood pressurerecommendation of 140/90 pre-dialy-sis and 130/80 in the CKD popula-tion (NKF, 2005). Nurses are oftenthe first to assess blood pressures inpatients on dialysis and evaluateresponse to changes in therapy.Patients may institute better compli-ance and demonstrate improvementsin blood pressure regulation with agreater understanding of the inherentrisk. With the high preponderance ofpatients beginning dialysis with car-diovascular disease, it is imperativethat clinicians make a more concertedeffort in treating the risks for cardio-vascular disease.

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Carol Headley, DNSc, RN, CNN and Barry M. Wall MDPosttest — 1.5 Contact Hours

Posttest Questions (See posttest instructions on the answer form, on page 28.)

1. What statement is true about the fluidbalance between the interstitium andthe 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 serveto protect the lung from fluid accumula-tion.

D. The lymphatic vessels continuouslyabsorb 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 lessefficient in removing fluid and there isincreased likelihood for development ofedema.

B. Acute elevations in left atrial pressureresult in pulmonary capillary pressureincreases and fluid is forced into theinterstitium and alveoli.

C. Elevated pulmonary capillary wedgepressure overwhelms the lymphaticsystem and edema results.

D. Increased pulse pressure and systolichypertension leads to decrease cardiacoutput 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 aredeleterious and lead to pulmonaryedema.

B. Initially stimulation of the sympatheticnervous system decreases cardiac out-put.

C. Stimulation of the RAAS causes saltand water excretion by the kidneys.

D. Long-term stimulation leads to myocyteapoptosis, hypertrophy, and myocardialnecrosis.

6. Diastolic dysfunction refers to a disor-der

A. of myocardial relaxation resulting inimpaired ventricular filling.

B. of myocardial stiffness that results indelayed ventricular emptying.

C. associated with left ventricular hyper-trophy and abnormal filling.

D. that occurs as a result of pressurechanges related to malfunctioningvalves.

7. There is a strong association between———- and the development of dias-tolic dysfunction and flash pulmonaryedema.

A. hypertensionB. left ventricular hypertrophyC. anemiaD. volume overload

8. The increased resistance to diastolicventricular 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 theprevalence of diastolic heart failure?

A. 50% of persons greater than age 60with CHF will have diastolic failure.

B. Prognosis for systolic heart failure isbetter than diastolic heart failure.

C. Patients over 70 years old with diastolicfailure have a 30% 5-year mortality.

D. Kidney disease contributes to thedevelopment of diastolic heart failure atearlier ages.

10. What statement is true about renalartery stenosis (RAS)?

A. Chronic mild to moderate hypertensionis associated with RAS.

B. It is seen in older women with fibro-muscular dysplasia.

C. It commonly involves atheroscleroticplague deposition in the renal artery.

D. It is always associated with a decreasein kidney function.

11. Your patient has a brain natriuretic pep-tide (BNP) level 700 pg/ml. What wouldyour next action be?

A. CT scan of the brainB. X-ray of the chestC. Administer hypertensive medicationsD. Complete a physical assessment

12. Common finding(s) on physical exami-nation of a patient with flash pulmonaryedema 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 unitsmay contribute to flash pulmonaryedema?

A. Holding BP medications pre-dialysisB. Inaccurate dry weight assessmentC. Use of non-tunneled catheters for dial-

ysisD. Eating on dialysis

14. Your patient arrives for dialysis withtachypnea, hypertension, and cracklesin the bases of the lungs. You feel thepatient has cardiogenic mediated flashpulmonary edema. Why?

A. Insignificant intradialytic weight gainonly

B. Insignificant intradialytic weight gainand absence of edema only

C. Insignificant intradialytic weight gain,absence of edema, and hypertensiononly

D. Insignificant intradialytic weight gain,absence of edema, and hypertensionand no history of ischemic heart dis-ease



ANSWER/EVALUATION FORMFlash Pulmonary Edema in Patients with Chronic Kidney Disease and

End Stage Renal DiseaseCarol M. Headley, DNSc, RN, and Barry M. Wall MD

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• Complete the evaluation.• Send only the answer form to the

ANNA National Office; East HollyAvenue Box 56; Pitman, NJ 08071-0056; or fax this form to (856) 589-7463.

• Enclose a check or money orderpayable to ANNA. Fees listed in pay-ment section.

• Posttests must be postmarked byFebruary 20, 2009. If you receive apassing score of 70% or better, acertificate for 1.5 contact hours willbe awarded by ANNA.

• Please allow 2-3 weeks for process-ing. You may submit multiple answerforms in one mailing, however,because of various processing pro-cedures for each answer form, youmay not receive all of your certificatesreturned in one mailing.

Note: If you wish to keep the journal intact, you may photocopy the answer sheet or access this posttest atwww.nephrologynursingjournal.net.

1. a b c d2. a b c d3. a b c d



10. a b c d11. a b c d12. a b c d

13. a b c d14. a b c d

Special NoteYour posttest can be processed in 1 week for an additional rush charge of $5.00.■■ Yes, I would like this posttest rush processed. I have included an additional fee of

$5.00 for rush processing.

Recognize the risk for development of flashpulmonary edema in patients with chronickidney disease and ESRD

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Flash Pulmonary Edema in Patients with Chronic Kidney ... · Flash Pulmonary Edema Flash pulmonary edema can origi-Flash Pulmonary Edema in Patients with Chronic Kidney Disease and