Pulmonary edema medical therapy
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
Medical Therapy
Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis.[1]
Cardiogenic pulmonary edema:
The main goal of management is to alleviate symptoms and stabilize patient as well as to improve outcome.[2]
Oxygen therapy
- Administer oxygen as early as possible
- Achieve 95% arterial oxygen saturation (90% in COPD patients)
- Caution should be taken in patients with severe airway obstruction to avoid hypercapnia
Drug therapy
- loop diuretics
- Recommended in the case of congestion and volume overload as the underlying cause of pulmonary edema
- The recommended initial dose is bolus furosemide 20 – 40 mg i.v. (0.5 – 1 mg bumetanide; 10 -20 mg torasemide)
- Total dose of furosemide is100 mg in the first 6 hours and 240 mg for the first 24 hours
- Thiazides combined with loop diuretics can be useful in cases resistant to diuretics
- In cases of acute cardiogenic pulmonary edema with volume overload, thiazides and aldosterone antagonists can be used in combination with loop diuretics
- A combination of drugs in low doses is more effective and has less side effects than the use of higher doses of a single drug
- Side Effects of Loop diuretics include:
- Hypokalemia
- Hyponatremia
- Hyperuricemia
- Hypovolemia
- Dehydration
- Urine output should be evaluate as frequent as possible
- Morphine and Its Analogues
- May be given in the early stage of the treatment in patient with severe acute heart failure, especially if they present with restlessness, dyspnea, anxiety, or chest pain[3]
- Relieves dyspnea and other symptoms
- Bolus of morphine 2.5 – 5 mg may be administered
- Respiration should be monitored
- Nausea often occurs and antiemetics therapy may be necessary
- Extra caution when giving morphine in following conditions:
- Hypotension
- Bradycardia
- Advanced AV block
- CO2 retention
- Vasopressin Antagonists
- Types of vasopressin receptors include:[3][4]
- V1a receptor which mediates vasoconstriction
- V2 receptor in the kidneys which its stimulation may induce water reabsorption.
- Two most studied vasopressin antagonists are conivaptan (dual V1a/v2 AVP receptor antagonist) in hyponatremia and tolvaptan (selective oral antagonist of V2 receptor) in acute heart failure (AHF).
- The EVEREST study suggests that tolvaptan relieves symptoms associated with acute heart failure and induces weight loss in acute phase but it does not reduce mortality or morbidity at 1 year
- Vasodilators
- Vasodilators are recommended at initial phase of ACPE without symptomatic hypotension, SBP <90 mmHg or serious obstructive valve disease
- Inotropic agents
- Dobutamine
- Dopamin
- Vasopressor
- Milrinone and Enoximone
- Cardiac Glycosides
References
- ↑ Murray JF (February 2011). "Pulmonary edema: pathophysiology and diagnosis". Int. J. Tuberc. Lung Dis. 15 (2): 155–60, i. PMID 21219673.
- ↑ Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.
- ↑ 3.0 3.1 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.
- ↑ 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.