Pulmonary edema medical therapy: Difference between revisions
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==Overview== | ==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== | ==Medical Therapy== | ||
Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis.<ref name="pmid21219673">{{cite journal |vauthors=Murray JF |title=Pulmonary edema: pathophysiology and diagnosis |journal=Int. J. Tuberc. Lung Dis. |volume=15 |issue=2 |pages=155–60, i |date=February 2011 |pmid=21219673 |doi= |url=}}</ref> | Pulmonary edema classified into cardiogenic and non-cardiogenic pulmonary edema, each requires different management and has a different prognosis.<ref name="pmid21219673">{{cite journal |vauthors=Murray JF |title=Pulmonary edema: pathophysiology and diagnosis |journal=Int. J. Tuberc. Lung Dis. |volume=15 |issue=2 |pages=155–60, i |date=February 2011 |pmid=21219673 |doi= |url=}}</ref><ref name="pmid16199340">{{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> | ||
=== Cardiogenic pulmonary edema: === | === Cardiogenic pulmonary edema: === | ||
The main goal of management is to alleviate symptoms and stabilize patient as well as to improve outcome.<ref name="pmid20973297">{{cite journal |vauthors=Alwi I |title=Diagnosis and management of cardiogenic pulmonary edema |journal=Acta Med Indones |volume=42 |issue=3 |pages=176–84 |date=July 2010 |pmid=20973297 |doi= |url=}}</ref> | The main goal of management is to alleviate symptoms and stabilize patient as well as to improve outcome.<ref name="pmid20973297">{{cite journal |vauthors=Alwi I |title=Diagnosis and management of cardiogenic pulmonary edema |journal=Acta Med Indones |volume=42 |issue=3 |pages=176–84 |date=July 2010 |pmid=20973297 |doi= |url=}}</ref> | ||
* The initial management of patients is following the ABCs of [[resuscitation]], that is, [[airway]], [[breathing]], and [[circulation]] | |||
* Any associated [[arrhythmia]] or [[myocardial infarction]] 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 ==== | ==== Oxygen therapy ==== | ||
| Line 17: | Line 25: | ||
* 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 [[hypercapnia]] | * 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 include: | |||
*** Bilevel positive airway pressure [BiPAP] | |||
*** 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<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''' | |||
** 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> | |||
** Can be used in sublingual, IV, or transdermal form | |||
** Should be avoided in hypotensive patient | |||
* '''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 | ||
| Line 33: | Line 54: | ||
*** [[Dehydration]] | *** [[Dehydration]] | ||
**** [[Urine output]] should be evaluate as frequent as possible | **** [[Urine output]] should be evaluate as frequent as possible | ||
* '''Morphine | * '''Morphine sulfate''' | ||
** 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]]<ref name="pmid18356349">{{cite journal |vauthors=Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL |title=Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis |journal=Emerg Med J |volume=25 |issue=4 |pages=205–9 |date=April 2008 |pmid=18356349 |doi=10.1136/emj.2007.050419 |url=}}</ref> | ** 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]]<ref name="pmid18356349">{{cite journal |vauthors=Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL |title=Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis |journal=Emerg Med J |volume=25 |issue=4 |pages=205–9 |date=April 2008 |pmid=18356349 |doi=10.1136/emj.2007.050419 |url=}}</ref> | ||
** Relieves [[dyspnea]] and other symptoms | ** Relieves [[dyspnea]] and other symptoms | ||
| Line 44: | Line 65: | ||
*** Advanced [[AV block]] | *** Advanced [[AV block]] | ||
*** [[CO2 retention]] | *** [[CO2 retention]] | ||
* '''Vasopressin Antagonists''' | * '''Nesiritide''' | ||
** Nesiritide is recombinant form of BNP use in patient with acute left heart failure and cardiogenic pulmonary edema<ref name="pmid10400005">{{cite journal |vauthors=Mills RM, LeJemtel TH, Horton DP, Liang C, Lang R, Silver MA, Lui C, Chatterjee K |title=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 |journal=J. Am. Coll. Cardiol. |volume=34 |issue=1 |pages=155–62 |date=July 1999 |pmid=10400005 |doi= |url=}}</ref> | |||
** Reduce pulmonary capillary wedge pressure | |||
** Increases in stroke volume | |||
** Increase cardiac index | |||
** Useful for patients in whom NTG is contraindicated (eg, patients taking sildenafil) | |||
==== 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:<ref name="pmid9482284">{{cite journal |vauthors=Gammage M |title=Treatment of acute pulmonary oedema: diuresis or vasodilatation? |journal=Lancet |volume=351 |issue=9100 |pages=382–3 |date=February 1998 |pmid=9482284 |doi=10.1016/S0140-6736(98)22006-X |url=}}</ref> | |||
* 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:<ref name="pmid24223323">{{cite journal |vauthors=Levy PD, Bellou A |title=Acute Heart Failure Treatment |journal=Curr Emerg Hosp Med Rep |volume=1 |issue=2 |pages= |date=June 2013 |pmid=24223323 |pmc=3821770 |doi=10.1007/s40138-013-0012-8 |url=}}</ref> | |||
** 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<ref name="pmid12749747">{{cite journal |vauthors=Moazemi K, Chana JS, Willard AM, Kocheril AG |title=Intravenous vasodilator therapy in congestive heart failure |journal=Drugs Aging |volume=20 |issue=7 |pages=485–508 |date=2003 |pmid=12749747 |doi= |url=}}</ref> | |||
* 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 | |||
* 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 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<ref name="pmid16181823">{{cite journal |vauthors=Bayram M, De Luca L, Massie MB, Gheorghiade M |title=Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes |journal=Am. J. Cardiol. |volume=96 |issue=6A |pages=47G–58G |date=September 2005 |pmid=16181823 |doi=10.1016/j.amjcard.2005.07.021 |url=}}</ref> | |||
** 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 | |||
* '''Dopamin''' | |||
** Stimulates the [[beta adrenergic receptor]] both directly and indirectly<ref name="pmid16181823" /> | |||
** 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]] | |||
* '''Norepinephrine''' | |||
** 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<ref name="pmid11191531">{{cite journal |vauthors=Galley HF |title=Renal-dose dopamine: will the message now get through? |journal=Lancet |volume=356 |issue=9248 |pages=2112–3 |date=2000 |pmid=11191531 |doi=10.1016/S0140-6736(00)03484-X |url=}}</ref> | |||
* 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]] | |||
'''Vasopressin Antagonists''' | |||
* Types of vasopressin receptors include:<ref name="pmid18356349" /><ref name="pmid17384437">{{cite journal |vauthors=Konstam MA, Gheorghiade M, Burnett JC, Grinfeld L, Maggioni AP, Swedberg K, Udelson JE, Zannad F, Cook T, Ouyang J, Zimmer C, Orlandi C |title=Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial |journal=JAMA |volume=297 |issue=12 |pages=1319–31 |date=March 2007 |pmid=17384437 |doi=10.1001/jama.297.12.1319 |url=}}</ref> | * Types of vasopressin receptors include:<ref name="pmid18356349" /><ref name="pmid17384437">{{cite journal |vauthors=Konstam MA, Gheorghiade M, Burnett JC, Grinfeld L, Maggioni AP, Swedberg K, Udelson JE, Zannad F, Cook T, Ouyang J, Zimmer C, Orlandi C |title=Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial |journal=JAMA |volume=297 |issue=12 |pages=1319–31 |date=March 2007 |pmid=17384437 |doi=10.1001/jama.297.12.1319 |url=}}</ref> | ||
** V1a receptor which mediates [[vasoconstriction]] | ** V1a receptor which mediates [[vasoconstriction]] | ||
** [[V2 receptor]] in the kidneys which induce water reabsorption | ** [[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 | |||
* | |||
* | '''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 === | ||
* Non-invasive ventilation (NIV) support [[ventilation]] without the use of an [[endotracheal tube]], but using a closed face mask instead<ref name="pmid209732972">{{cite journal |vauthors=Alwi I |title=Diagnosis and management of cardiogenic pulmonary edema |journal=Acta Med Indones |volume=42 |issue=3 |pages=176–84 |date=July 2010 |pmid=20973297 |doi= |url=}}</ref> | |||
* 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]] [[Acute respiratory distress syndrome medical therapy|click here]]. | |||
==== High-altitude pulmonary edema ==== | |||
For more information about treatment of [[Altitude sickness|high-altitude]] pulmonary edema [[Altitude sickness medical therapy|click here]]. | |||
==References== | ==References== | ||
Latest revision as of 19:27, 15 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. 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]
- The initial management of patients is following the ABCs of resuscitation, that is, airway, breathing, and circulation
- Any associated arrhythmia or myocardial infarction 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 include:
- Bilevel positive airway pressure [BiPAP]
- 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
- 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
- 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 sulfate
- 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
- Nesiritide
- Nesiritide is recombinant form of BNP use in patient with acute left heart failure and cardiogenic pulmonary edema[7]
- Reduce pulmonary capillary wedge pressure
- Increases in stroke volume
- Increase cardiac index
- Useful for patients in whom NTG is contraindicated (eg, patients taking sildenafil)
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
- 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 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
- Dopamin
- Stimulates the beta adrenergic receptor both directly and indirectly[11]
- 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
- Norepinephrine
- 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[12]
- 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
Vasopressin Antagonists
- Types of vasopressin receptors include:[6][13]
- 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
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
- Non-invasive ventilation (NIV) support ventilation without the use of an endotracheal tube, but using a closed face mask instead[14]
- 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Moazemi K, Chana JS, Willard AM, Kocheril AG (2003). "Intravenous vasodilator therapy in congestive heart failure". Drugs Aging. 20 (7): 485–508. PMID 12749747.
- ↑ 11.0 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.
- ↑ 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.
- ↑ 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.
- ↑ Alwi I (July 2010). "Diagnosis and management of cardiogenic pulmonary edema". Acta Med Indones. 42 (3): 176–84. PMID 20973297.