Pulmonary edema: Difference between revisions

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==Background==
==Background==
*Cardiogenic vs Non-Cardiogenic (ARDS/Altitude/Neurogenic)
{{Pulmonary edema types}}
*Mechanism of Cardiogenic
**Failing heart > pulm edema > stress response > incr afterload
***Incr afterload > incr pulm edema
*Pts often intravascularly depleted; avoid diuretics!
 
==Causes==
*[[Congestive heart failure|Cardiogenic]]
*Non-cardiogenic
**Hypertensive crisis.
*[[Negative pressure pulmonary edema]] (Upper airway obstruction)
*Neurogenic causes
**[[Seizures]]
**[[Blunt head trauma]]
**[[Strangulation]]
**[[Electrocution]]
*Other
**[[ARDS]]
**Inhalation of hot or toxic gases
**[[Pulmonary contusion]]
**Aspiration
**Reexpansion edema (post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Immersion pulmonary edema[7][8]
Multiple blood transfusions
Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS.
There are also a range of causes of pulmonary edema which are less well characterised and arguably represent specific instances of the broader classifications above.
 
Arteriovenous malformation
Hantavirus pulmonary syndrome
High altitude pulmonary edema (HAPE), probably a manifestation of neurogenic pulmonary edema[9][10]
Envenomation, such as with the venom of Atrax robustus[11]
Flash pulmonary edema
Swimming induced pulmonary edema
 
 
 
==Diagnosis==
*Crackles
*Respiratory distress


==Clinical Features==
{{Pulmonary edema clinical features}}
==Differential Diagnosis==
==Differential Diagnosis==
{{SOB DDX}}
{{SOB DDX}}


==Treatment==
==Evaluation==
#CPAP/BiPAP with PEEP 6-8; titrate up to PEEP of 10-12
[[File:PedalEdema.jpg|thumb|Pitting pedal edema]]
#Nitroglycerin
[[File:PulmEdema.png|thumb|Pulmonary edema with small pleural effusions on both sides.]]
##Dosing Options
[[File:Pulmonary Edema Bowra.gif|thumbnail|POCUS shows B lines<ref>http://www.thepocusatlas.com/pulmonary/</ref>]]
###Sublingual 0.4 mg q5min
*CBC (rule out anemia)
###Nitropaste (better bioavailability than oral Nitroglycerin)
*Chem
###Intravenous: 0.1mcg/kg/min - 5mcg/kg/min
*Albumin level
*[[ECG]]
*[[CXR]]
**Cephalization
**Interstitial edema
**Pulmonary venous congestion
**Pleural effusion
**Alveolar edema
**Cardiomegaly
*[[Troponin]] +/- BNP
*[[Ultrasound]]
**Bedside to assess [[Cardiac ultrasound|global function]], [[Ultrasound: lungs|B lines]], [[IVC ultrasound|assessment of IVC]]
**Formal TTE/TEE
 
{{BNP value}}
{{Lung ultrasound pulmonary edema}}


''Generally start IV Nitroglycerin 50mcg/min and titrate rapidly (150mcg/min or higher)to symptom relief''
==Management==
*CPAP/[[BiPAP]] with PEEP 6-8; titrate up to PEEP of 10-12
*[[Nitroglycerin]]
**Dosing Options
***Sublingual 0.4mg q5min
***Nitropaste (better bioavailability than oral Nitroglycerin)
***Intravenous: 0.1mcg/kg/min - 5mcg/kg/min
****Generally start IV nitroglycerin 50mcg/min and titrate rapidly (150mcg/min or higher) to symptom relief as long as patient's blood pressure tolerates
*If [[nitroglycerin]] fails to reduce work of breathing, consider nitroprusside (reduces both preload and afterload) or ACE-inhibitiors (preload reducer)
*After patient improves, titrate down [[nitroglycerin]] as [[enalaprilat]] (0.625 - 1.25mg IV) or [[captopril]] are started
*Morphine is no longer recommended due to increased morbidity<ref>Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J. 2008 Apr;25(4):205-9.</ref><ref>Ellingsrud C, Agewall S. Morphine in the treatment of acute pulmonary oedema--Why? Int J Cardiol. 2016 Jan 1;202:870-3.</ref>


*If NTG fails to reduce BP consider nitroprusside (reduces both preload and afterload) or ACE-inhibitiors (preload reducer)
==Disposition==
*After pt improves titrate down NTG as enaliprilat (0.625 - 1.25mg IV) or captopril are started
*Depends on underlying cause, hemodynamic stability, and response to treatment
*Morphine is no longer recommended do to increased morbidity


==See Also==
==See Also==
*[[Congestive Heart Failure (CHF)]]
*[[Congestive heart failure]]
*[[Acute Respiratory Distress Syndrome]]
*[[Acute Respiratory Distress Syndrome]]
*[[Flash pulmonary edema]]


==References==
==References==
<references/>  
<references/>  


[[Category:Cards]]
[[Category:Cardiology]]
[[Category:Pulm]]
[[Category:Pulmonary]]

Latest revision as of 00:15, 8 September 2021

Background

Pulmonary Edema Types

Pulmonary capillary wedge pressure <18 mmHg differentiates noncardiogenic from cardiogenic pulmonary edema[1]

Clinical Features

Differential Diagnosis

Acute dyspnea

Emergent

Non-Emergent

Evaluation

Pitting pedal edema
Pulmonary edema with small pleural effusions on both sides.
POCUS shows B lines[2]

Brain natriuretic peptide (BNP)[3]

  • Measurement
    • <100 pg/mL: Negative for acute CHF (Sn 90%, NPV 89%)
    • 100-500 pg/mL: Indeterminate (Consider differential diagnosis and pre-test probability)
    • >500 pg/mL: Positive for acute CHF (Sp 87%, PPV 90%)
    • Combination of BNP with clinician judgment 94% sensitive 70% specific (compared to 49% sn and 96% spec clinical judgement alone) [4]

NT-proBNP[5][6][7]

  • <300 pg/mL → CHF unlikely
  • CHF likely in:
    • >450 pg/mL in age < 50 years old
    • >900 pg/mL in 50-75 years old
    • >1800 pg/mL in > 75 years old

Lung ultrasound of pulmonary edema

Lung ultrasound showing pulmonary edema.
  • A lines and B lines
    • A lines:
      • Appear as horizontal lines
      • Indicate dry interlobular septa.
      • Predominance of A lines has 90% sensitivity, 67% specificity for pulmonary artery wedge pressure <= 13mm Hg
      • A line predominance suggests that intravenous fluids may be safely given without concern for pulmonary edema
    • B lines ("comets"):
      • White lines from the pleura to the bottom of the screen
      • Highly sensitive for pulmonary edema, but can be present at low wedge pressures

Management

  • CPAP/BiPAP with PEEP 6-8; titrate up to PEEP of 10-12
  • Nitroglycerin
    • Dosing Options
      • Sublingual 0.4mg q5min
      • Nitropaste (better bioavailability than oral Nitroglycerin)
      • Intravenous: 0.1mcg/kg/min - 5mcg/kg/min
        • Generally start IV nitroglycerin 50mcg/min and titrate rapidly (150mcg/min or higher) to symptom relief as long as patient's blood pressure tolerates
  • If nitroglycerin fails to reduce work of breathing, consider nitroprusside (reduces both preload and afterload) or ACE-inhibitiors (preload reducer)
  • After patient improves, titrate down nitroglycerin as enalaprilat (0.625 - 1.25mg IV) or captopril are started
  • Morphine is no longer recommended due to increased morbidity[8][9]

Disposition

  • Depends on underlying cause, hemodynamic stability, and response to treatment

See Also

References

  1. ↑ Clark SB, Soos MP. Noncardiogenic Pulmonary Edema. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 1, 2020.
  2. ↑ http://www.thepocusatlas.com/pulmonary/
  3. ↑ Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167. doi:10.1056/NEJMoa020233.
  4. ↑ McCullough et al. B-Type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from breathing not properly (BNP) multinational study. Circulation. 2002:DOI: 10.1161/01.CIR.0000025242.79963.4
  5. ↑ Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. Eur Heart J. 2006 Feb. 27(3):330-7.
  6. ↑ Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med. 2005 Feb 17. 352(7):666-75.
  7. ↑ Moe GW, Howlett J, Januzzi JL, Zowall H,. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation. 2007 Jun 19. 115(24):3103-10.
  8. ↑ Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J. 2008 Apr;25(4):205-9.
  9. ↑ Ellingsrud C, Agewall S. Morphine in the treatment of acute pulmonary oedema--Why? Int J Cardiol. 2016 Jan 1;202:870-3.
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