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 induce water reabsorption
- 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
- Vasodilators
- Vasodilators are recommended at initial phase of acute cardiogenic pulmonary edema
- Intravenous nitrate
- Sodium nitroprusside
- Use vasodilators in acute cardiogenic pulmonary edema when
- SBP > 110 mmHg
- The initial recommended dose of intravenous nitroglycerin is 10 – 20 ug/minutes, which can be increased to 5 – 10 ug/minute every 3 – 5 minutes if required.
- These drugs lower SBP, reduce left and right-heart filling pressure and systemic vascular resistance, as well as relieving dyspnea. Coronary blood flow is usually maintained unless the diastolic pressure is disturbed
- Vasodilators relieve pulmonary congestion in APE, usually without compromising stroke volume or increasing myocardial oxygen demand, particularly in patients with acute coronary syndrome
- Calcium antagonists are not recommended in the treatment of APE.
- Patients with aortic stenosis may experience overt hypotension following administration of intravenous vasodilator drugs.
- Titrating nitroglycerin i.v. gradually and monitoring blood pressure regularly are recommended to prevent drastic SBP decrease. Arterial line is not routinely required, but it will facilitate titration in patients with borderline blood pressure.
- Intravenous nitroprusside must be given with caution. Initial infusion rate is 0.3 ug/kg/minute with titration up to 5 ug/kg/minute.
- Intravenous nesiritide can be given with or without bolus infusion with infusion rate ranging from 0.015 to 0.03 ug/kg/minute. Noninvasive blood pressure monitoring is usually adequate. Combination with other intravenous vasodilators is not recommended
- Side Effects of Vasodilators include:
- Headache
- Tachyphylaxis
- Hypotension
- 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.