Pulmonary edema: Difference between revisions

No edit summary
 
(44 intermediate revisions by 8 users not shown)
Line 1: Line 1:
==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!


==Diagnosis==
==Clinical Features==
*Crackles
{{Pulmonary edema clinical features}}
*Respiratory distress
==Differential Diagnosis==
{{SOB DDX}}


==Specific types==
==Evaluation==
*Negative pressure pulmonary edema
[[File:PedalEdema.jpg|thumb|Pitting pedal edema]]
**Forced inspiration against obstructed airway causes large negative intrathoracic pressure, leading to pulmonary edema<ref>Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011 Jul-Sep; 5(3): 308–313.</ref>
[[File:PulmEdema.png|thumb|Pulmonary edema with small pleural effusions on both sides.]]
**Mostly due to postoperative laryngospasm, sudden drops in PEEP (high PEEP to manual BVM), trauma such as hanging, strangulation, foreign bodies, etc.
[[File:Pulmonary Edema Bowra.gif|thumbnail|POCUS shows B lines<ref>http://www.thepocusatlas.com/pulmonary/</ref>]]
**Diagnosis
*CBC (rule out anemia)
***Hypoxemia (may be sudden and large - beware "fake" or "not real" SpO2), stridor, retractions, accessory muscle use, crackles/wheezes
*Chem
***CXR shows diffuse interstitial and alveolar infiltrates
*Albumin level
***CT shows preferential central/nondependent distribution of edema (as opposed to other forms of pulmonary edema)
*[[ECG]]
**Treatment
*[[CXR]]
***Relieve airway obstruction
**Cephalization
***Vent with generous PEEP and diuretics
**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


==Treatment==
{{BNP value}}
#CPAP/BiPAP with PEEP 6-8; titrate up to PEEP of 10-12
{{Lung ultrasound pulmonary edema}}
#Nitroglycerin
##Dosing Options
###Sublingual 0.4 mg 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''
==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


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


==Source==
==References==
Tintinalli
 
EMCrit Podcast 1
 
<references/>  
<references/>  


[[Category:Cards]]
[[Category:Cardiology]]
[[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.