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Acute Pulmonary Edema

Background

Definition: Accumulation of blood in the pulmonary vasculature as a result of the

inability of the left ventricle to pump blood forward adequately. Acute pulmonary

edema, congestive heart failure (https://coreem.net/core/congestive-heart-

failure/) and cardiogenic shock (https://coreem.net/core/cardiogenic-shock/) are

a spectrum of diseases and should be considered and managed differently.

Epidemiology:

5 Million patients diagnosed with CHF in the US

500,000 new CHF diagnoses each year in the US

Unclear what percentage of these patients will present with acute pulmonary

edema (APE)

Causes: Acute myocardial infarction (AMI) is the most common cause of APE but

there are a multitude of other causes including acute valvular pathology.

Pathophysiology: Our understanding of the pathophysiology of APE has changed

dramatically over the last 70 years. The current model is based on the effects of

neurohormones:

Primary myocardial injury (AMI) or stress leads to decreased arterial blood

pressure and renal perfusion

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(https://coreem.net/content/uploads/2015/06/Neurohormonal.png)

Decreased arterial blood pressure causes sympathetic activation and release of

neurohormones (i.e. norepinephrine).

Decreased renal perfusion activates the renin-angiotensin-aldoserone system

(RAAS)

Increased circulating neurohormones cause peripheral vasoconstriction

(increased afterload) and cardiotoxicity leading to secondary myocardial injury

Splanchnic vasoconstriction leads to redistribution of blood contributing to

increased preload and eventually, pulmonary volume overload

Symptoms

Shortness of breath

Dyspnea on exertion

Diaphoresis

Cough with pink sputum

Chest pain

Signs

Air hunger

Hypoxia

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Tachycardia

JVD

Rales

Skin pallor/mottling

Altered Mental Status

Decreased Urine Output

Immediate Management:

NB: Patients with APE have extremely tenuous respiratory status. As such, early

management choices (first 10 minutes) determine whether these patients have

good or bad outcomes.

Basics: ABCs, IV, O , Cardiac Monitor, 12-lead EKG and POC Lung Ultrasound

Breathing

Severe respiratory distress typically present and increased work of breathing

can lead to fatigue as well as worsening cardiac function

Apply non-invasive positive pressure ventilation (NIPPV)

Multiple effects including decreasing work of breathing and stenting open

alveoli during the entire respiratory cycle leading to improved gas exchange.

NIPPV has been shown to reduce the need for intubation by decreasing work

of breathing (Nava 2003 (https://www.ncbi.nlm.nih.gov/pubmed/12958051),

Bersten 1991 (https://www.ncbi.nlm.nih.gov/pubmed/1961221))

Limited evidence demonstrates an advantage of bilevel positive airway

pressure (BPAP) over continuous positive airway pressure (CPAP) (Liesching

2014 (https://www.ncbi.nlm.nih.gov/pubmed/24071031))

Circulation

APE patients will have severely elevated blood pressures resulting from

sympathetic activation and resultant vasoconstriction.

Despite elevated blood pressures, end organ hypoperfusion occurs due to

marked arterial vasoconstriction. This leads to acute kidney injury (AKI),

intestinal ischemia, coronary ischemia and brain hypoperfusion.

2

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The lungs in a patient with APE are like an overflowing bathtub. We have to

simultaneously stop the inflow of blood by turning off the tap (preload

reduction) and increase outflow by unclogging the drain (afterload reduction)

12-Lead EKG

Obtain an EKG as soon as possible to help identify etiologies of APE with

specific indicated interventions.

(https://coreem.net/content/uploads/2015/06/APE-

CXR-Radpod.jpg)

Acute Pulmonary Edema –radpod.com

Myocardial ischemia and infarction are common causes of APE that EKG can

rapidly identify.

Life-threatening tachydysrhythmias may cause APE or occur due to ischemia.

Chest X-Ray (CXR)

May be helpful in confirming clinical diagnosis and in ruling out other possible

etiologies.

Most common finding: bilateral pulmonary congestion

Point of Care Ultrasound (POCUS)

Point of Care Ultrasound (POCUS)POCUS is an important diagnostic modality in patients with suspected APE

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(https://coreem.net/content/uploads/2015/09/zcb0060817370003.jpeg)

B-Lines Seen on Lung Ultrasound

In patients with APE, POCUS will demonstrate the presence of “B-lines”The presence of > 3 B-lines per rib space suggests the presence of

interstitial pulmonary fluid.

Read More: Lichtenstein’s BLUE Protocol

(https://www.ncbi.nlm.nih.gov/pubmed/18403664)

Severe respiratory distress can be caused by a number of etiologies

Presenting symptoms and signs overlap

Diagnoses may be difficult to differentiate clinically

Alternate diagnoses: asthma/COPD exacerbation, pulmonary embolism,

pneumothorax

Evidence demonstrates that physicians more accurately identify pulmonary

edema on lung US than with CXR (Martindale 2012

(https://www.ncbi.nlm.nih.gov/pubmed/23263648)).

A recent RCT demonstrated superiority of lung US in determining the final

diagnosis of a patient presenting with undifferentiated respiratory distress

(Laursen et al. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/24998674)).

Additionally, POCUS may identify a ruptured valve causing the patient’s

symptoms leading to an alternate management pathway (i.e. cardiovascular

surgery for valve repair)

Read More: US Against the World (http://boringem.org/2015/01/19/us-world-

ultrasound-differentiating-copd-chf/): Ultrasound in Differentiating COPD from

CHF (Boring EM)

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Lung US - Pulmonary Edemafrom Core EM

00:10

Directed Treatment

Nitroglycerin (NTG)

(https://coreem.net/content/uploads/2015/09/TNT.jpeg)

Low dose nitrates (< 100 mcg/min): cause venodilation leading to decreased

preload

High dose nitrates (> 100 mcg/min): cause arterial dilation reducing afterload

Can be given sublingual while IV access is being obtained (Bussman 1978

(https://www.ncbi.nlm.nih.gov/pubmed/417614))

If patient tolerates sublingual well, can start IV dosing at 50-75 mcg/min and

titrate up rapidly

Angiotensin Converting Enzyme Inhibitor (ACEI)

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Proposed mechanism: Interrupting the RAAS system leading to decreased

neurohormonal drive. Leads to decreased afterload.

Limited evidence demonstrates increased patient respiratory comfort and

non-statistically significant decreases in respiratory failure (Hamilton 1996

(https://www.ncbi.nlm.nih.gov/pubmed/8673775)).

ACEI are often unnecessary after aggressive NTG dosing

Less Useful Treatments

Morphine

Classic teaching from medical school endorses treatment of APE with “MONA”– Morphine, Oxygen, Nitroglycerin and Aspirin.

Retrospective analysis of the Acute Decompensated Heart Failure Registry

(ADHERE) database demonstrated an association between the use of

morphine and increased mortality and ICU admission rate. (Peacock 2008

(https://www.ncbi.nlm.nih.gov/pubmed/18356349))

Read More: Morphine Kills in Acute Decompensated Heart Failure

(http://rebelem.com/morphine-kills-in-acute-decompensated-heart-failure/)

(REBEL EM)

Loop Diuretics (i.e. furosemide)

More than 50% of patients presenting in APE do not have volume overload but

rather have volume redistribution (Zile 2008

(https://www.ncbi.nlm.nih.gov/pubmed/18794390), Chaudhry 2007

(https://www.ncbi.nlm.nih.gov/pubmed/17846286), Fallick 2011

(https://www.ncbi.nlm.nih.gov/pubmed/21934091)).

Additionally, many patients with APE and volume overload will also have

ESRD making loop diuretics noneffective in eliminating volume.

Loop diuretics decrease glomeluar filtration rate (GFR), activate the RAAS,

decrease cardiac output and increase afterload early after administration

(Marik 2012 (https://www.ncbi.nlm.nih.gov/pubmed/21616957)).

Read More: Furosemide in the Treatment of Acute Pulmonary Edema

(http://www.emdocs.net/furosemide-treatment-acute-pulmonary-edema/)

(emDocs.net)

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Take Home Points

1. APE, CHF exacerbation and cardiogenic shock are different diseases and

must be approached and treated differently.

2. In patients presenting with undifferentiated respiratory distress, POCUS may

be extremely helpful in rapidly determining the underlying disease.

3. NIPPV should be rapidly applied to patients to support oxygenation and

ventilation.

4. Start nitrates early and rapidly titrate up to reduce both preload and

afterload.

References:

Nava S et al. Noninvasive ventilation in cardiogenic pulmonary edema – a multicenter randomized trial.Am J Resp Crit Care Med 2003; 168: 1432-7. PMID: 12958051(https://www.ncbi.nlm.nih.gov/pubmed/12958051)

Bersten AD et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airwaypressure delivered by face mask. NEJM 1991; 325 (26): 1825-30. PMID: 1961221(https://www.ncbi.nlm.nih.gov/pubmed/1961221)

Liesching T et al. Randomized trial of bilevel versus continuous positive airway pressure for acutepulmonary edema. J Emerg Med 2014; 46(1): 130-40. PMID: 24071031(https://www.ncbi.nlm.nih.gov/pubmed/24071031)

Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: TheBLUE protocol. Chest 2008; 134: 117-25. PMID: 18403664 (https://www.ncbi.nlm.nih.gov/pubmed/18403664)

Martindale JL et al. Diagnosing pulmonary edema: lung ultrasound versus chest radiography. Eur JEmerge Med 2012. PMID: 23263648 (https://www.ncbi.nlm.nih.gov/pubmed/23263648)

Laursen CB et al. Point-of-care ultrasonography in patients admitted with respiratory symptoms: a single-blind, randomised controlled trial. Lancet Respir Med 2014; 2: 638-46. PMID: 24998674(https://www.ncbi.nlm.nih.gov/pubmed/24998674)

Bussmann W, Schupp D. Effect of sublingual nitroglycerin in emergency treatment of severe pulmonaryedema. Am J Card 1978; 41: 931-936. PMID: 417614 (https://www.ncbi.nlm.nih.gov/pubmed/417614)

Hamilton RJ et al. Rapid Improvement of acute pulmonary edema with sublingual captopril. Acad EmergMed 1996; 3: 205-12. PMID: 8673775 (https://www.ncbi.nlm.nih.gov/pubmed/8673775)

Haude M et al. Sublingual administration of captopril versus nitroglycerin in patients with severecongestive heart failure. Intl J Card 1990; 27: 351-9. PMID: 2112516(https://www.ncbi.nlm.nih.gov/pubmed/2112516)

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Peacock WF et al. Morphine and Outcomes in Acute Decompensated Heart Failure: An ADHEREAnalysis. Emerg Med J 2008; 25: 205 – 209. PMID: 18356349(https://www.ncbi.nlm.nih.gov/pubmed/18356349)

Zile MR et al. Transition from chronic compensated to acute decompensated heart failure:pathophysiological insights obtained from continuous monitoring of intracardiac pressures. Circulation2008; 118: 1433-41. PMID: 18794390 (https://www.ncbi.nlm.nih.gov/pubmed/18794390)

Chaudhry S et al. Patterns of weight change preceding hospitalization for heart failure. Circulation2007;116:1549 –54. PMID: 17846286 (https://www.ncbi.nlm.nih.gov/pubmed/17846286)

Fallick C et al. Sympathetically mediated changes in capacitance: redistribution of the venous reservoir asa cause of decompensation. Circ Heart Fail 2011; 4: 669-75. PMID: 21934091(https://www.ncbi.nlm.nih.gov/pubmed/21934091)

Marik PE, Flemmer M. Narrative review: the management of acute decompensated heart failure. JIntensive Care Med 2012; 27: 343-53. PMID: 21616957 (https://www.ncbi.nlm.nih.gov/pubmed/21616957)

(https://coreem.net/author/anand-

swaminathan/)

@emswami (https://twitter.com/@emswami)

See My Posts(https://coreem.net/author/anand-swaminathan/)

Anand Swaminathan, MD, MPHAnand "Swami" Swaminathan is an assistant professor of

Emergency Medicine in the Ronald O. Perelman

Emergency Department and assistant residency director

of the NYU/Bellevue Emergency Medicine residency

program. His interests are in resuscitation medicine,

resident education and cutting the knowledge

translation window. Swami is an active contributor and

supporter of innovations in medicine, particularly Free

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contributor to a number of sites including ALiEM, LITFL,

ERCast, and The SGEM. Swami is an associate editor for

REBEL EM and REBEL Cast. He is also faculty for the

Essentials of Emergency Medicine and Deputy Editor of

EM: RAP.

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