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

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.

Cardiogenic pulmonary edema:

The main goal of management is to alleviate symptoms and stabilize patient as well as to improve outcome.

• 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

• Nitroglycerin
  • Nitroglycerin is the most effective and rapid medication for reducing preload
  • 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
  • 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
  • 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:

• 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:
  • 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

• 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
  • 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
  • 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
• 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:
  • 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

• 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.