acute pulmonary edema - irp-cdn.multiscreensite.com
TRANSCRIPT
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 1/11
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
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 2/11
(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
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 3/11
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
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 4/11
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
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 5/11
(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)
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 6/11
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)
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 7/11
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)
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 8/11
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)
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 9/11
Leave a Reply
Your email address will not be published. Required fields are marked *
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
Open Access Medical Education (FOAM). He is a
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.
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 10/11
COMMENT
NAME *
EMAIL *
WEBSITE
Post Comment
Type search here . . .
NYU Langone Health is one of the nation’s premier academic medical centers whose mission is to serve, teach,
and discover.
About Core EM
Core EM is dedicated to bringing Emergency Providers all things core content Emergency Medicine. In the true
spirit of Emergency Medicine our content is available to anyone, anywhere, anytime.
Quick Links
2/26/2020 Acute Pulmonary Edema – Core EM
https://coreem.net/core/ape/ 11/11
About Core EM (https://coreem.net/about-us/)
Recommended Sites (https://coreem.net/recommended/)
Core EM Podcast (https://coreem.net/podcast/)
Disclaimer / Privacy (https://coreem.net/disclaimer-privacy-policy/)
Contact Us (https://coreem.net/contact-us/)
(https://twitter.com/Core_EM) (https://www.facebook.com/coreem.net)
(https://www.youtube.com/c/CoreEM) (https://coreem.net/feed/)
Get In Touch
Have feedback? Suggestions on how we can improve the site? Click below to contact us or find us on Twitter,
Facebook or Google+
Copyright © 2015—2020 Core EM