Pulmonary edema medical therapy: Difference between revisions
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* Methods of oxygen delivery include: | * Methods of oxygen delivery include: | ||
** Use of a [[face mask]] | ** Use of a [[face mask]] | ||
** Noninvasive pressure-support [[ventilation]] (which includes [[bilevel positive airway pressure]] [BiPAP] and continuous [[positive airway pressure]] | ** Noninvasive pressure-support [[ventilation]] (which includes [[bilevel positive airway pressure]] [BiPAP] and continuous [[positive airway pressure]] [CPAP]) | ||
** [[Intubation]] | ** [[Intubation]] | ||
** [[Mechanical ventilation]] | ** [[Mechanical ventilation]] | ||
====Preload reduction==== | ====Preload reduction==== | ||
Preload reduction is used as first line of treatment to reduce right-heart filling pressures and pulmonary capillary hydrostatic pressures | Preload reduction is used as first line of treatment to reduce right-heart filling pressures and pulmonary capillary hydrostatic pressures<ref name="pmid161993402">{{cite journal |vauthors=Mattu A, Martinez JP, Kelly BS |title=Modern management of cardiogenic pulmonary edema |journal=Emerg. Med. Clin. North Am. |volume=23 |issue=4 |pages=1105–25 |date=November 2005 |pmid=16199340 |doi=10.1016/j.emc.2005.07.005 |url=}}</ref> | ||
* '''Nitroglycerin''' | |||
** can be used in sublingual, IV, or transdermal form | |||
** Nitroglycerin is the most effective and rapid medication for reducing preload<ref name="pmid9924848">{{cite journal |vauthors=Beltrame JF, Zeitz CJ, Unger SA, Brennan RJ, Hunt A, Moran JL, Horowitz JD |title=Nitrate therapy is an alternative to furosemide/morphine therapy in the management of acute cardiogenic pulmonary edema |journal=J. Card. Fail. |volume=4 |issue=4 |pages=271–9 |date=December 1998 |pmid=9924848 |doi= |url=}}</ref> | |||
* '''loop diuretics''' | * '''loop diuretics''' | ||
** Recommended in the case of [[congestion]] and volume overload as the underlying cause of pulmonary edema | ** Recommended in the case of [[congestion]] and volume overload as the underlying cause of pulmonary edema | ||
Revision as of 14:04, 9 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
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. Treatment that may required includes: vasodilators when the blood pressure is normal or high, diuretics if there is excess volume or fluid retention, inotropic agents in patients with hypotension and signs of organ hypoperfusion. Intubation and mechanical ventilation may be required to achieve adequate oxygenation.
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]
- The initial management of patients is following the ABCs of resuscitation, that is, airway, breathing, and circulation.
- Any associated arrhythmia or MI should be treated appropriately.
- After initial management, medical treatment of cardiogenic pulmonary edema focuses on following main goals:
- Reduction of pulmonary venous return (preload reduction)
- Reduction of systemic vascular resistance (afterload reduction)
- Inotropic support
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
- Methods of oxygen delivery include:
- Use of a face mask
- Noninvasive pressure-support ventilation (which includes bilevel positive airway pressure [BiPAP] and continuous positive airway pressure [CPAP])
- Intubation
- Mechanical ventilation
Preload reduction
Preload reduction is used as first line of treatment to reduce right-heart filling pressures and pulmonary capillary hydrostatic pressures[4]
- Nitroglycerin
- can be used in sublingual, IV, or transdermal form
- Nitroglycerin is the most effective and rapid medication for reducing preload[5]
- 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[6]
- 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:[6][7]
- 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[8]
- 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
- Intravenous nitrate
- Vasodilators effects include:
- lowering systolic blood pressure
- Reducing left and right-heart filling pressure
- Reducing systemic vascular resistance
- Relieving dyspnea
- Use vasodilators in acute cardiogenic pulmonary edema when:
- SBP > 110 mmHg
- Side effects of Vasodilators include:
- Headache
- Tachyphylaxis
- Hypotension
- Titrating nitroglycerin i.v. gradually and monitoring blood pressure regularly to prevent sudden decrease in systolic blood pressure
- Inotropic agents
- 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
- Dobutamine
- Positive inotropic agent acting through stimulation of β1-receptors[9]
- 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
- Dobutamine
- Dopamin
- Stimulates the beta adrenergic receptor both directly and indirectly[9]
- Must be used with caution in patients with heart rate of 100 times/min
- Low dose dopamine infusion (2-3 ug/kg/min) stimulates dopaminergic receptor
- At higher dose may stimulate a-adrenergic through vasoconstriction may be used to maintain the systolic blood pressure, but there is an increasing risk of tachycardia and arrhythmia
- Dopamin
- Vasopressor
- Vasopressors (i.e. norepinephrine) are not recommended for first-line therapy
- Indicated in cardiogenic shock when the use of an inotropic agent combined with fluid challenge fail to restore systolic blood pressure over 90 mmHg
- Type III phosphodiesterease inhibitors (PDEIs)
- Milrinone and enoximone are the two type III phosphodiesterease inhibitors (PDEIs) used in clinical practice[10]
- type III phosphodiesterease inhibitors (PDEIs) effects include:
- Inhibit degradation of cyclic AMP
- Inotropic effect
- Peripheral vasodilating
- Increase in cardiac output and stroke volume
- Decrease pulmonary artery pressure
- Decrease pulmonary wedge pressure
- Decrease systemic and pulmonary vascular resistance
- Cardiac Glycosides
- Cause slight increase on cardiac output and decreased filling pressure
- May be useful to decrease ventricular rate in acute cardiogenic pulmonary edema
Indication for Non-invasive Ventilation
- Non-invasive ventilation (NIV) support ventilation without the use of an endotracheal tube, but using a closed face mask instead[11]
- 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 with PEEP improves left ventricle function by reducing left ventricle afterload
- 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
- ↑ Murray JF (February 2011). "Pulmonary edema: pathophysiology and diagnosis". Int. J. Tuberc. Lung Dis. 15 (2): 155–60, i. PMID 21219673.
- ↑ 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.
- ↑ Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.
- ↑ 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.
- ↑ 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.
- ↑ 6.0 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.
- ↑ 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.
- ↑ Moazemi K, Chana JS, Willard AM, Kocheril AG (2003). "Intravenous vasodilator therapy in congestive heart failure". Drugs Aging. 20 (7): 485–508. PMID 12749747.
- ↑ 9.0 9.1 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.
- ↑ 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.
- ↑ Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.