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Respiratory Failure Medication

  • Author: Ata Murat Kaynar, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
 
Updated: Mar 31, 2015
 

Medication Summary

Pharmacotherapy for cardiogenic pulmonary edema and acute exacerbations of chronic obstructive pulmonary disease (COPD) is discussed here. The goals of therapy in cardiogenic pulmonary edema are to achieve a pulmonary capillary wedge pressure of 15-18 mm Hg and a cardiac index greater than 2.2 L/min/m2 while maintaining adequate blood pressure and organ perfusion. These goals may have to be modified for some patients. Diuretics, nitrates, analgesics, and inotropes are used in the treatment of acute pulmonary edema.

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Diuretics, Other

Class Summary

First-line therapy generally includes a loop diuretic such as furosemide, which inhibits sodium chloride reabsorption in the ascending loop of Henle.

Furosemide (Lasix)

 

Administer loop diuretics such as furosemide intravenously (IV) because this allows both superior potency and a higher peak concentration despite an increased incidence of adverse effects, particularly ototoxicity.

Metolazone (Zaroxolyn)

 

Metolazone has been used as adjunctive therapy in patients initially refractory to furosemide. It has been demonstrated to be synergistic with loop diuretics in treating refractory patients and causes a greater loss of potassium. Metolazone is a potent thiazide-related diuretic that sometimes is used in combination with furosemide for more aggressive diuresis. It is also used for initiating diuresis in patients with a degree of renal dysfunction.

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Nitrates

Class Summary

Nitrates reduce myocardial oxygen demand by lowering preload and afterload. In severely hypertensive patients, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, in view of the possibility of thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside, IV nitroglycerin may be the initial therapy of choice for afterload reduction.

Nitroglycerin sublingual (Nitro-Bid, NitroMist, Nitrostat, Nitrolingual)

 

Sublingual nitroglycerin tablets and spray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. As with sublingual nitroglycerin tablets, the onset of action of nitroglycerin spray is 1-3 minutes, with a half-life of 5 minutes. Administration of the spray may be easier, and it can be stored for as long as 4 years.

Topical nitrate therapy is reasonable in a patient presenting with class I-II congestive heart failure (CHF). However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred because it is easier to monitor hemodynamics and absorption, particularly in patients with diaphoresis. Oral nitrates, because of their delayed absorption, play little role in the management of acute pulmonary edema.

Nitroprusside sodium (Nitropress)

 

Nitroprusside produces vasodilation of venous and arterial circulation. At higher dosages, it may exacerbate myocardial ischemia by increasing heart rate. It is easily titratable.

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Opioid Analgesics

Class Summary

Morphine IV is an excellent adjunct in the management of acute pulmonary edema. In addition to anxiolysis and analgesia, its most important effect is venodilation, which reduces preload. It also causes arterial dilatation, which reduces systemic vascular resistance and may increase cardiac output.

Morphine sulfate (Duramorph, Astramorph)

 

Morphine sulfate is the drug of choice for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated until the desired effect is obtained.

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Inotropic Agents

Class Summary

The principal inotropic agents are dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In patients with hypotension who present with CHF, dopamine and dobutamine usually are employed. Inamrinone and milrinone inhibit phosphodiesterase, resulting in increased intracellular cyclic adenosine monophosphate (cAMP) and altered calcium transport. As a result, they increase cardiac contractility and reduce vascular tone by vasodilatation.

Dopamine

 

Dopamine is a positive inotropic agent that stimulates both adrenergic and dopaminergic receptors. Its hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation; higher doses produce cardiac stimulation and renal vasodilation. Doses of 2-10 µg/kg/min can lead to tachycardia, ischemia, and dysrhythmias. Doses higher than 10 µg/kg/min cause vasoconstriction, which increases afterload.

Norepinephrine (Levophed)

 

Norepinephrine is used in protracted hypotension after adequate fluid replacement. It stimulates beta1- and alpha-adrenergic receptors, which leads to increased cardiac muscle contractility and heart rate, as well as vasoconstriction. As a result, norepinephrine increases systemic blood pressure and cardiac output. Adjust and maintain infusion to stabilize blood pressure (eg, 80-100 mm Hg systolic) sufficiently to perfuse vital organs.

Dobutamine

 

Dobutamine produces vasodilation and increases the inotropic state. At higher dosages, it may cause increased heart rates, thus exacerbating myocardial ischemia. It is a strong inotropic agent with minimal chronotropic effect and no vasoconstriction.

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Beta2 Agonists

Class Summary

Bronchodilators are an important component of treatment in respiratory failure caused by obstructive lung disease. These agents act to decrease muscle tone in both small and large airways in the lungs. This category includes beta-adrenergics, methylxanthines, and anticholinergics.

Terbutaline (Brethaire, Bricanyl)

 

Terbutaline acts directly on beta2 receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.

Albuterol (Proventil)

 

Albuterol is a beta-agonist useful in the treatment of bronchospasm. It selectively stimulates beta2-adrenergic receptors of the lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

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Xanthine Derivatives

Class Summary

Xanthine derivatives may relax smooth muscle of the bronchi.

Theophylline (Elixophyllin Elixir, Theo-24)

 

Theophylline has a number of physiologic effects, including increases in collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. It partially acts by inhibiting phosphodiesterase, elevating cellular cAMP levels, or antagonizing adenosine receptors in the bronchi, resulting in relaxation of smooth muscle. However, its clinical efficacy is controversial, especially in the acute setting.

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Anticholinergics, Respiratory

Class Summary

Anticholinergics antagonize the action of acetylcholine with muscarinic receptor on bronchial smooth muscle.

Ipratropium bromide (Atrovent HFA)

 

Ipratropium bromide is an anticholinergic medication that appears to inhibit vagally mediated reflexes by antagonizing the action of acetylcholine, specifically with the muscarinic receptor on bronchial smooth muscle. Vagal tone can be significantly increased in COPD; therefore, this can have a profound effect. Ipratropium can be combined with a beta-agonist because it may require 20 minutes to begin having an effect.

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Corticosteroids

Class Summary

Corticosteroids have been shown to be effective in accelerating recovery from acute COPD exacerbations and are an important anti-inflammatory therapy in asthma. Although they may not make a clinical difference in the emergency department (ED), they have some effect 6-8 hours into therapy; therefore, early dosing is critical.

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

 

Methylprednisolone is usually given IV in the ED for initiation of corticosteroid therapy, although in theory, oral administration should be equally efficacious.

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Contributor Information and Disclosures
Author

Ata Murat Kaynar, MD Associate Professor, Departments of Critical Care Medicine and Anesthesiology, University of Pittsburgh School of Medicine

Ata Murat Kaynar, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Chest Physicians, American Society of Anesthesiologists, Society of Critical Care Medicine, Society of Critical Care Anesthesiologists

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership; Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board membership.

Acknowledgements

Cory Franklin, MD Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Harold L Manning, MD Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School

Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Khan NA, Palepu A, Norena M, et al. Differences in hospital mortality among critically ill patients of Asian, Native Indian, and European descent. Chest. 2008 Dec. 134(6):1217-22. [Medline].

  2. Moss M, Mannino DM. Race and gender differences in acute respiratory distress syndrome deaths in the United States: an analysis of multiple-cause mortality data (1979- 1996). Crit Care Med. 2002 Aug. 30(8):1679-85. [Medline].

  3. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000 May 4. 342(18):1301-8. [Medline].

  4. Phua J, Badia JR, Adhikari NK, et al. Has mortality from acute respiratory distress syndrome decreased over time?: A systematic review. Am J Respir Crit Care Med. 2009 Feb 1. 179(3):220-7. [Medline].

  5. Noveanu M, Breidthardt T, Reichlin T, Gayat E, Potocki M, Pargger H, et al. Effect of oral beta-blocker on short and long-term mortality in patients with acute respiratory failure: results from the BASEL-II-ICU study. Crit Care. 2010 Nov 3. 14(6):R198. [Medline]. [Full Text].

  6. Canet E, Osman D, Lambert J, et al. Acute respiratory failure in kidney transplant recipients: a multicenter study. Crit Care. 2011 Mar 8. 15(2):R91. [Medline].

  7. Peek GJ, Elbourne D, Mugford M, Tiruvoipati R, Wilson A, Allen E, et al. Randomised controlled trial and parallel economic evaluation of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR). Health Technol Assess. 2010 Jul. 14(35):1-46. [Medline].

  8. Girault C, Briel A, Benichou J, Hellot MF, Dachraoui F, Tamion F, et al. Interface strategy during noninvasive positive pressure ventilation for hypercapnic acute respiratory failure. Crit Care Med. 2009 Jan. 37(1):124-31. [Medline].

  9. Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010 Mar 3. 303(9):865-73. [Medline].

  10. Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med. 1995 Sep 28. 333(13):817-22. [Medline].

  11. Plant PK, Owen JL, Elliott MW. Early use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentre randomised controlled trial. Lancet. 2000 Jun 3. 355(9219):1931-5. [Medline].

  12. Vitacca M, Clini E, Rubini F, Nava S, Foglio K, Ambrosino N. Non-invasive mechanical ventilation in severe chronic obstructive lung disease and acute respiratory failure: short- and long-term prognosis. Intensive Care Med. 1996 Feb. 22(2):94-100. [Medline].

  13. Confalonieri M, Potena A, Carbone G, Porta RD, Tolley EA, Umberto Meduri G. Acute respiratory failure in patients with severe community-acquired pneumonia. A prospective randomized evaluation of noninvasive ventilation. Am J Respir Crit Care Med. 1999 Nov. 160(5 Pt 1):1585-91. [Medline].

  14. Antonelli M, Conti G, Rocco M, et al. A comparison of noninvasive positive-pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med. 1998 Aug 13. 339(7):429-35. [Medline].

 
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Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting.
A 44-year-old woman developed acute respiratory failure and diffuse bilateral infiltrates. She met the clinical criteria for the diagnosis of acute respiratory distress syndrome. In this case, the likely cause was urosepsis.
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A Bilevel positive airway pressure support machine is shown here. This could be used in spontaneous mode or timed mode (backup rate could be set).
Headgear and full face mask commonly are used as the interface for noninvasive ventilatory support.
Bilevel positive airway pressure (BiPAP) and inspiratory positive airway pressure (IPAP) settings are shown. IPAP or expiratory positive airway pressure (EPAP) and frequency can be preset.
Noninvasive ventilation with bilevel positive airway pressure for acute respiratory failure secondary to exacerbation of chronic obstructive pulmonary disease.
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Lung biopsy on this patient with acute respiratory failure and diffuse pulmonary infiltrates helped yield the diagnosis of pulmonary edema. Therefore, cardiogenic pulmonary edema should be excluded as the cause of respiratory failure prior to considering lung biopsy.
Pressure-volume curve of a patient with acute respiratory distress syndrome (ARDS) on mechanical ventilation can be constructed. The lower and the upper ends of the curve are flat, and the central portion is straight (where the lungs are most compliant). For optimal mechanical ventilation, patients with ARDS should be kept between the inflection and the deflection point.
Surgical lung biopsy was performed in the patient described in Image 3. The histology shows features of diffuse alveolar damage, including epithelial injury, hyperplastic type II pneumocytes, and hyaline membranes.
 
 
 
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