Pulmonary edema medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]

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Overview

Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis.The main goal of a treatment are alleviate symptoms and improving hemodynamics. The initial management of patients is following the ABCs of resuscitation, that is, airway, breathing, and circulation. Medical treatment of cardiogenic pulmonary edema focuses on preload reduction, afterload reduction and inotropic support.

Medical Therapy

Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis.[1][2]

Cardiogenic pulmonary edema:

The main goal of management is to alleviate symptoms and stabilize patient as well as to improve outcome.[3]

Oxygen therapy

Preload reduction

Preload reduction is used as first line of treatment to reduce right-heart filling pressures and pulmonary capillary hydrostatic pressures[4]

  • Nitroglycerin
    • Nitroglycerin is the most effective and rapid medication for reducing preload[5]
    • Can be used in sublingual, IV, or transdermal form
    • Should be avoided in hypotensive patient

Afterload reduction

Elevated level of catecholamine in cardiogenic pulmonary edema patient cause increase in systemic vascular resistanced afterload

  • ACE inhibitors

 The use of ACE inhibitors in cardiogenic pulmonary edema is associated with following:[8]

  • Reduced admission rates to ICUs
  • Decreased endotracheal intubation rates
  • Decreased length of ICU stay
  • Captopril and enalapril are two forms of ACEIs given in cardiogenic pulmonary edema cause the following effect:[9]
    • Reductions in systemic vascular resistance (afterload)
    • Improvements in PCWP (preload)
    • Increase stroke volume
    • Increase cardiac output
  • Vasodilators

Vasodilators are recommended at initial phase of acute cardiogenic pulmonary edema[10]

  • Intravenous nitrate
    • The initial recommended dose is 10 – 20 ug/minutes, which can be increased to 5 – 10 ug/minute every 3 – 5 minutes if required
  • Sodium nitroprusside
    • The Initial infusion rate is 0.3 ug/kg/minute with titration up to 5 ug/kg/minute

Inotropic support

Inotropic agents should be considered in patients with following conditions:

  • low output condition with signs of hypoperfusion
  • Congestion despite vasodilators and/or diuretics
  • Should be given in patients with hypokinetic and enlarged ventricle
  • Should be given immediately and stop rapidly when hemodynamic condition of patients improve
  • May acutely improve hemodynamic and clinical condition of patients with acute cardiogenic pulmonary edema
  • May lead to further myocardial injury and increased short-term and long-term mortality

Two main classes of inotropic agents are available:

  • Catecholamine agents
    • Dobutamine
    • Dopamin
    • Norepinephrine
  • Phosphodiesterase inhibitors (PDIs)
  • Dobutamine
    • Positive inotropic agent acting through stimulation of β1-receptors[11]
    • Given with an infusion rate of 2-3 ug/kg/min without a loading dose
    • The elimination of the drug is rapid after ending of infusion
    • Blood pressure must always be monitored
    • Used with caution in patients with heart rate of 100 times/min
  • Norepinephrine
  • Type III phosphodiesterease inhibitors (PDEIs)

Vasopressin Antagonists

  • Two most studied vasopressin antagonists are:
    • Conivaptan (dual V1a/v2 AVP receptor antagonist)
    • Tolvaptan (selective oral antagonist of V2 receptor)

Tolvaptan relieves symptoms associated with acute heart failure but it does not reduce mortality or morbidity at 1 year

Cardiac Glycosides

  • Cause the slight increase in cardiac output and decreased filling pressure
  • Maybe useful to decrease ventricular rate in acute cardiogenic pulmonary edema

Indication for Non-invasive Ventilation

  • NIV with positive end-expiratory pressure (PEEP) should be used as early as possible in every patient with acute cardiogenic pulmonary edema and hypertensive acute heart failure
  • NIV should be used with caution in cardiogenic shock and right ventricle failure

Non-cardiogenic pulmonary edema

Acute respiratory distress syndrome

For more information about treatment of acute respiratory distress syndrome click here.

High-altitude pulmonary edema

For more information about treatment of high-altitude pulmonary edema click here.

References

  1. Murray JF (February 2011). "Pulmonary edema: pathophysiology and diagnosis". Int. J. Tuberc. Lung Dis. 15 (2): 155–60, i. PMID 21219673.
  2. Mattu A, Martinez JP, Kelly BS (November 2005). "Modern management of cardiogenic pulmonary edema". Emerg. Med. Clin. North Am. 23 (4): 1105–25. doi:10.1016/j.emc.2005.07.005. PMID 16199340.
  3. Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.
  4. Mattu A, Martinez JP, Kelly BS (November 2005). "Modern management of cardiogenic pulmonary edema". Emerg. Med. Clin. North Am. 23 (4): 1105–25. doi:10.1016/j.emc.2005.07.005. PMID 16199340.
  5. Beltrame JF, Zeitz CJ, Unger SA, Brennan RJ, Hunt A, Moran JL, Horowitz JD (December 1998). "Nitrate therapy is an alternative to furosemide/morphine therapy in the management of acute cardiogenic pulmonary edema". J. Card. Fail. 4 (4): 271–9. PMID 9924848.
  6. 6.0 6.1 Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL (April 2008). "Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis". Emerg Med J. 25 (4): 205–9. doi:10.1136/emj.2007.050419. PMID 18356349.
  7. Mills RM, LeJemtel TH, Horton DP, Liang C, Lang R, Silver MA, Lui C, Chatterjee K (July 1999). "Sustained hemodynamic effects of an infusion of nesiritide (human b-type natriuretic peptide) in heart failure: a randomized, double-blind, placebo-controlled clinical trial. Natrecor Study Group". J. Am. Coll. Cardiol. 34 (1): 155–62. PMID 10400005.
  8. Gammage M (February 1998). "Treatment of acute pulmonary oedema: diuresis or vasodilatation?". Lancet. 351 (9100): 382–3. doi:10.1016/S0140-6736(98)22006-X. PMID 9482284.
  9. Levy PD, Bellou A (June 2013). "Acute Heart Failure Treatment". Curr Emerg Hosp Med Rep. 1 (2). doi:10.1007/s40138-013-0012-8. PMC 3821770. PMID 24223323.
  10. Moazemi K, Chana JS, Willard AM, Kocheril AG (2003). "Intravenous vasodilator therapy in congestive heart failure". Drugs Aging. 20 (7): 485–508. PMID 12749747.
  11. 11.0 11.1 Bayram M, De Luca L, Massie MB, Gheorghiade M (September 2005). "Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes". Am. J. Cardiol. 96 (6A): 47G–58G. doi:10.1016/j.amjcard.2005.07.021. PMID 16181823.
  12. Galley HF (2000). "Renal-dose dopamine: will the message now get through?". Lancet. 356 (9248): 2112–3. doi:10.1016/S0140-6736(00)03484-X. PMID 11191531.
  13. Konstam MA, Gheorghiade M, Burnett JC, Grinfeld L, Maggioni AP, Swedberg K, Udelson JE, Zannad F, Cook T, Ouyang J, Zimmer C, Orlandi C (March 2007). "Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial". JAMA. 297 (12): 1319–31. doi:10.1001/jama.297.12.1319. PMID 17384437.
  14. Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.