Pulmonary edema medical therapy: Difference between revisions
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==== Oxygen therapy ==== | ==== Oxygen therapy ==== | ||
* Administer oxygen as early as possible | * Administer [[oxygen]] as early as possible | ||
* Achieve 95% arterial oxygen saturation (90% in COPD patients) | * Achieve 95% [[arterial oxygen saturation]] (90% in [[COPD]] patients) | ||
* Caution should be taken in patients with severe airway obstruction to avoid | * Caution should be taken in patients with severe [[airway obstruction]] to avoid [[hypercapnia]] | ||
==== Drug therapy ==== | ==== Drug therapy ==== | ||
* '''loop diuretics''' | * '''loop diuretics''' | ||
** Recommended in the case of | ** 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) | ** 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 | ** 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 | ** [[Thiazide|Thiazides]] combined with [[loop diuretics]] can be useful in cases resistant to diuretics | ||
** In cases of acute cardiogenic pulmonary edema with volume overload, thiazides | ** 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 | ** 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: | ** Side Effects of [[Loop diuretics]] include: | ||
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*** Advanced AV block | *** Advanced AV block | ||
*** CO2 retention | *** CO2 retention | ||
* Vasopressin Antagonists | * '''Vasopressin Antagonists''' | ||
* Vasodilators | * Some types of vasopressin receptors have been identified: V1a receptor which mediates vasoconstriction and 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 | ||
* Inotropic agents | * '''Vasodilators''' | ||
* Dobutamine | * Vasodilators are recommended at initial phase of ACPE without symptomatic hypotension, SBP <90 mmHg or serious obstructive valve disease | ||
* Dopamin | * '''Inotropic agents''' | ||
* Vasopressor | * '''Dobutamine''' | ||
* Milrinone and Enoximone | * '''Dopamin''' | ||
* Cardiac Glycosides | * '''Vasopressor''' | ||
* '''Milrinone and Enoximone''' | |||
* '''Cardiac Glycosides''' | |||
==References== | ==References== |
Revision as of 21:05, 6 March 2018
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
- Some types of vasopressin receptors have been identified: V1a receptor which mediates vasoconstriction and 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.
- ↑ 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.