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Respiratory Failure: Treatment & Medication

Author: Ata Murat Kaynar, MD, Assistant Professor, Departments of Critical Care Medicine and Anesthesiology, University of Pittsburgh School of Medicine
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
Contributor Information and Disclosures

Updated: May 20, 2009

Treatment

Medical Care

Hypoxemia is the major immediate threat to organ function. Therefore, the first objective in the management of respiratory failure is to reverse and/or prevent tissue hypoxia. Hypercapnia unaccompanied by hypoxemia generally is well tolerated and probably is not a threat to organ function unless accompanied by severe acidosis. Many experts believe that hypercapnia should be tolerated until the arterial blood pH falls below 7.2. Appropriate management of the underlying disease obviously is an important component in the management of respiratory failure.

A patient with acute respiratory failure generally should be admitted to a respiratory care or intensive care unit. Most patients with chronic respiratory failure can be treated at home with oxygen supplementation and/or ventilatory assist devices along with therapy for their underlying disease.

• Airway management
  • Assurance of an adequate airway is vital in a patient with acute respiratory distress.
  • The most common indication for endotracheal intubation (ETT) is respiratory failure.
  • ETT serves as an interface between the patient and the ventilator.
  • Another indication for ETT is airway protection in patients with altered mental status.
• Correction of hypoxemia
  • After securing an airway, attention must turn to correcting the underlying hypoxemia, the most life-threatening facet of acute respiratory failure.
  • The goal is to assure adequate oxygen delivery to tissues, generally achieved with a PaO₂ of 60 mm Hg or an arterial oxygen saturation (SaO₂) of greater than 90%.
  • Supplemental oxygen is administered via nasal prongs or face mask; however, in patients with severe hypoxemia, intubation and mechanical ventilation are often required.
• Coexistent hypercapnia and respiratory acidosis may need to be addressed. This is done by correcting the underlying cause or providing ventilatory assistance.
  • Mechanical ventilation is used for 2 essential reasons: (1) to increase PaO₂ and (2) to lower PaCO₂. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue.
• Ventilator management
  • The use of mechanical ventilation during the polio epidemics of the 1950s was the impetus that led to the development of the discipline of critical care medicine.
  • Prior to the mid 1950s, negative-pressure ventilation with the use of iron lungs was the predominant method of ventilatory support.
  • Currently, virtually all mechanical ventilatory support for acute respiratory failure is provided by positive-pressure ventilation. Nevertheless, negative-pressure ventilation still is used occasionally in patients with chronic respiratory failure.
  • Over the years, mechanical ventilators have evolved from simple pressure-cycled machines to sophisticated microprocessor-controlled systems. A brief review of mechanical ventilation is presented as follows.
• Overview of mechanical ventilation
  • Positive-pressure versus negative-pressure ventilation: In order for air to enter the lungs, a pressure gradient must exist between the airway and alveoli. This can be accomplished either by raising pressure at the airway (positive-pressure ventilation) or by lowering pressure at the level of the alveolus (negative-pressure ventilation). The iron lung or tank ventilator is the most common type of negative-pressure ventilator used in the past. These ventilators work by creating subatmospheric pressure around the chest, thereby lowering pleural and alveolar pressure, and thus facilitating flow of air into the patient's lungs. These ventilators are bulky, poorly tolerated, and are not suitable for use in modern critical care units. Positive-pressure ventilation can be achieved by an endotracheal or tracheostomy tube or noninvasively through a nasal mask or face mask.
  • Controlled versus patient-initiated (ie, assisted): Ventilatory assistance can be controlled (AC) or patient-initiated. In controlled modes of ventilation, the ventilator delivers assistance independent of the patient's own spontaneous inspiratory efforts. In contrast, during patient-initiated modes of ventilation, the ventilator delivers assistance in response to the patient's own inspiratory efforts. The patient's inspiratory efforts can be sensed either by pressure or flow-triggering mechanisms (see Triggering mechanism, below).
  • Pressure-targeted versus volume-targeted: During positive-pressure ventilation, either pressure or volume may be set as the independent variable. In volume-targeted (or volume preset) ventilation, tidal volume is the independent variable set by the physician and/or respiratory therapist, and airway pressure is the dependent variable. In volume-targeted ventilation, airway pressure is a function of the set tidal volume and inspiratory flow rate, the patient's respiratory mechanics (compliance and resistance), and the patient's respiratory muscle activity. In pressure-targeted (or pressure preset) ventilation, airway pressure is the independent variable and tidal volume is the dependent variable. The tidal volume during pressure-targeted ventilation is a complex function of inspiratory time, the patient's respiratory mechanics, and the patient's own respiratory muscle activity.
• Interface between patient and ventilator (mask vs endotracheal intubation)
  • Mechanical ventilation requires an interface between the patient and the ventilator. In the past, this invariably occurred through an endotracheal or tracheostomy tube, but in recent years, an increasing trend has occurred towards noninvasive ventilation, which can be accomplished by the use of either a full face mask (covering both the nose and mouth) or a nasal mask (see Noninvasive ventilatory support, below).⁵
  • Care of an endotracheal tube includes correct placement of the tube, maintenance of proper cuff pressure, and suctioning to maintain a patent airway.
  • Following intubation, the position of the tube in the airway (rather than esophagus) should be confirmed by auscultation of the chest and, ideally, by a carbon dioxide detector. As a general rule, the endotracheal tube should be inserted to an average depth of 23 cm in men and 21 cm in women (measured at the incisor). Confirming proper placement of the endotracheal tube with a chest radiograph is recommended.
  • The tube should be secured to prevent accidental extubation or migration into the mainstem bronchus, and the endotracheal tube cuff pressure should be monitored periodically. The pressure in the cuff generally should not exceed 25 mm Hg.
  • Endotracheal suctioning can be accomplished by either open-circuit or closed-circuit suction catheters. Routine suctioning is not recommended because suctioning may be associated with a variety of complications, including desaturation, arrhythmias, bronchospasm, severe coughing, and introduction of secretions into the lower respiratory tract.
• Specific modes of ventilatory support
  • Pressure support ventilation (PSV): PSV can be categorized as patient-initiated, pressure-targeted ventilation. With PSV, ventilatory assistance occurs only in response to the patient's spontaneous inspiratory efforts. With each inspiratory effort, the ventilator raises airway pressure by a preset amount. When the inspiratory flow rate decays to a minimal level or to a percentage of initial inspiratory flow (eg, 25% of peak flow), inspiration is terminated. During PSV, the patients are free to choose their own respiratory rate; inspiratory time, inspiratory flow rate, and tidal volume are determined, in part, by the patient's respiratory efforts. This mode of ventilation should not be used in patients with unstable ventilatory drive, and care must be exercised when the patient's respiratory mechanics are changing because of bronchospasm, secretions, or varying levels of auto–positive end-expiratory pressure (auto-PEEP).
  • Intermittent mandatory ventilation (IMV): IMV is a mode whereby mandatory breaths are delivered at a set frequency, tidal volume, and inspiratory flow rate. However, the patient can breathe spontaneously between the machine-delivered breaths. Most modern ventilators have synchronized IMV (SIMV), whereby the ventilator attempts to deliver the mandatory breaths in synchrony with the patient's own inspiratory efforts. In essence, the ventilator allows the patient an opportunity to breathe. If the patient makes an inspiratory effort during a window of time determined by the IMV rate, the ventilator delivers a mandatory breath in response to the patient's inspiratory effort. However, if no inspiratory effort is detected by the ventilator, a time-triggered breath is delivered. Compared with IMV, SIMV may improve patient comfort and may limit dynamic hyperinflation, which may occur when a preset breath is delivered immediately after the patient's spontaneous inspiratory effort (ie, prior to exhalation).
  • Assist-control ventilation: In assist-control ventilation, patients receive a fixed tidal volume and inspiratory flow rate with each inspiratory effort, regardless of their respiratory rate. However, a "back-up rate" is selected that guarantees that the patient receives a minimum number of breaths per minute. If the patient's respiratory rate falls below the back-up rate, the ventilator delivers the number of breaths necessary to reach the back-up rate; such breaths are delivered independently of any inspiratory effort by the patient.
  • Volume-control: In this mode, respiratory rate, tidal volume, and inspiratory flow rate (or inspiratory time) are fixed. This mode is used most often in heavily sedated or paralyzed patients.
  • Pressure-control: In contrast to volume control, in pressure-control mode, airway pressure is raised by a set amount at a fixed number of times per minute. The physician or respiratory therapist also sets the inspiratory-to-expiratory (I:E) ratio or the inspiratory time. This mode is used most often in heavily sedated or paralyzed patients.
  • Pressure-control inverse-ratio ventilation (PCIRV): PCIRV is a variation of simple pressure-control ventilation. In this mode, inspiration is set to be longer than expiration. The I:E ratio should rarely, if ever, exceed 3:1.
• Triggering mechanism: pressure versus flow triggering
  • In patient-initiated (assisted) ventilation, the ventilator must sense the patient's inspiratory effort in order to deliver assistance. Ventilator triggering may be based on either a pressure or a flow change.
  • With pressure-triggering, the ventilator is set to detect a certain change in pressure. The ventilator is triggered whenever airway pressure drops by the set amount. For example, in a patient on no positive end-expiratory pressure (PEEP) with a trigger sensitivity set at 1 cm water, a breath is triggered whenever airway pressure falls below -1 cm water. In a patient on 5-cm water PEEP with the same trigger sensitivity, a breath is triggered whenever airway pressure falls below +4 cm water.
  • In flow-triggering, a continuous flow of gas is sent through the ventilator circuit. In some ventilators, this continuous flow rate may be set by the physician or respiratory therapist, whereas in other ventilators, the continuous flow rate is fixed. A flow sensitivity is selected, and the ventilator senses the patient's inspiratory efforts by detecting a change in flow. When the patient makes an inspiratory effort, some of the gas that was previously flowing continuously through the circuit is diverted to the patient. The ventilator senses the decrease in flow returning through the circuit, and a breath is triggered. One problem with flow-triggering is that autotriggering sometimes results from leaks in the ventilator circuit.
• Positive end-expiratory pressure
  • By maintaining airway (and hence alveolar) pressure greater than zero, PEEP may recruit atelectatic alveoli and prevent their collapse during the succeeding expiration. PEEP also shifts lung water from the alveoli into the perivascular interstitial space and helps with recruitment of alveoli. However, it does not decrease the total amount of extravascular lung water.
  • In patients with disorders such as acute respiratory distress syndrome (ARDS) or acute lung injury, PEEP is applied to recruit atelectatic alveoli, thereby improving oxygenation and allowing a reduction in FiO₂ to nontoxic levels (FiO₂ <0.6). Applying PEEP of 3-5 cm water to prevent a decrease in functional residual capacity in patients with normal lungs is a common practice.
  • In an ARDS Network trial, higher PEEP produced better oxygenation and lung compliance but no benefit to survival, time on ventilator, or nonpulmonary organ dysfunction. Although sufficient PEEP is essential in ventilator management of patients with acute respiratory distress syndrome (ARDS), this level varies from patient to patient. Ideal PEEP helps to achieve adequate oxygenation and decrease the requirement for high fractions of inspiratory oxygen without causing any of the harmful effects of PEEP. Current evidence does not support routine application of high PEEP strategy in people with ALI or acute respiratory distress syndrome (ARDS).
  • PEEP causes an increase in intrathoracic pressure, which may decrease venous return and cardiac output, particularly in patients with hypovolemia.
• Inspiratory flow
  • In volume-targeted ventilation, inspiratory flow is a variable that is set by the physician or respiratory therapist. The inspiratory flow rate is selected on the basis of a number of factors, including the patient's inspiratory drive and the underlying disease.
  • Two flow patterns are used commonly: (1) a constant-flow (ie, square-wave) pattern and (2) a decelerating-flow pattern. With a constant-flow pattern, inspiratory flow is held constant throughout the breath, whereas with a decelerating-flow pattern, flow rises quickly to a maximal value and then decreases progressively throughout the breath.
  • In pressure-targeted ventilation, the inspiratory flow rate is a dependent variable that varies as a function of the preset pressure and the patient's own inspiratory effort. Because airway pressure is held constant while alveolar pressure rises during inspiration, the pressure difference between airway and alveoli decreases, leading to a decelerating pattern of inspiratory flow.
• Determinants of ventilator-associated lung injury
  • Mechanical ventilation is associated with a variety of insults to the lung.
  • In the past, physicians focused on barotrauma, including pneumothorax, pneumomediastinum, and subcutaneous and pulmonary interstitial emphysema. The manifestations of barotrauma likely occur because of excessive alveolar wall stress. Excessive airway pressure by itself does not appear to cause barotrauma. In critically ill patients, the manifestations of barotrauma can be subtle. For example, the earliest sign of pneumothorax in supine patients may be the deep-sulcus sign or a collection of air anteriorly along cardiophrenic angle.
  • More recently, lung damage indistinguishable from acute respiratory distress syndrome (ARDS) has been recognized to possibly be caused by certain patterns of ventilatory support. Early experiments in animals showed that mechanical ventilation employing high peak airway pressures and high tidal volume led to the formation of pulmonary edema. The mechanism was thought to be due to direct parenchymal injury and altered microvascular permeability secondary to high peak alveolar pressures. Recently, other investigators have shown that excessive tidal volumes resulting in alveolar overdistension are the most important factor in ventilator-associated lung injury.
  • A strategy of using low tidal volumes in patients with acute respiratory distress syndrome (ARDS) who are on mechanical ventilation has led to a reduced incidence of barotrauma and improved survival rates in recently published clinical trials.
• Mechanical ventilation in specific diseases
  • General guidelines
    • The mode of ventilation should be suited to the needs of the patient. Following the initiation of mechanical ventilation, the ventilator settings should be adjusted based on the patient's lung mechanics, underlying disease process, gas exchange, and response to mechanical ventilation.
    • SIMV and assist-control ventilation often are used for the initiation of mechanical ventilation.
    • In patients with intact respiratory drive and mild-to-moderate respiratory failure, PSV may be a good initial choice.
  • Supplemental oxygen
    • The lowest FiO₂ that produces an SaO₂ greater than 90% and a PaO₂ greater than 60 mm Hg generally is recommended.
    • The prolonged use of FiO₂ less than 0.6 is unlikely to cause pulmonary oxygen toxicity.
  • Acute respiratory distress syndrome
    • The primary objective is to accomplish adequate gas exchange while avoiding excessive inspired oxygen concentrations and alveolar overdistension.
    • The traditional ventilatory strategy of delivering high tidal volumes leads to high end-inspiratory alveolar pressures (ie, plateau pressure).
    • Many investigators currently believe that repeated cycles of opening and collapsing of inflamed and atelectatic alveoli are detrimental to the lung. Failure to maintain a certain minimum alveolar volume may further accentuate the lung damage. Furthermore, transalveolar pressure (reflected by plateau pressure) exceeding 25-30 cm water is considered to be an important risk factor for stretch injury to the lungs.
    • Patients with acute respiratory distress syndrome (ARDS) should be targeted to receive a tidal volume of 6 mL/kg. Importantly, remember that the set tidal volume should be based on ideal rather than actual body weight. If the plateau pressure remains excessive (>30 cm water), further reductions in tidal volume may be necessary.
    • ARDSNet, a prospective randomized clinical trial, demonstrated a striking reduction in hospital mortality in patient with acute respiratory distress syndrome (ARDS) who were ventilated with 6 mL/kg predicted body weight compared with 12 mL/kg. Patients who received the lower tidal volume strategy also had more ventilator-free and organ failure-free days. In the lower tidal volume group, the target tidal volume was 6 mL/kg of predicted body weight. This strategy may lead to respiratory acidosis, which requires either high respiratory rates and or sodium bicarbonate infusion.¹
    • Application of PEEP sufficient to raise the tidal volume above the lower inflection point (Pflex) on the pressure-volume curve may minimize alveolar wall stress and improve oxygenation. A pressure-volume curve can be constructed for an individual patient by measuring plateau pressures at different lung volumes. Pflex is the point at which the slope of the curve changes, indicating that the lung is operating at the most compliant part of the curve.
    • A lung-protective strategy in which the PaCO₂ is allowed to rise (permissive hypercapnia) may reduce barotrauma and enhance survival.
    • In some patients with acute respiratory distress syndrome (ARDS), the prone position may lead to significant improvements in oxygenation; whether this translates to improved outcome is unknown.
  • Obstructive airway diseases
    • In patients with COPD or asthma, institution of mechanical ventilation may worsen dynamic hyperinflation (auto-PEEP or intrinsic PEEP [PEEPi]). The dangers of auto-PEEP include a reduction in cardiac output and hypotension (because of decreased venous return) and barotrauma.
    • The goals of mechanical ventilation in obstructive airway diseases are to unload the respiratory muscles, achieve adequate oxygenation, and minimize the development of dynamic hyperinflation and its associated adverse consequences.
    • Following the initiation of mechanical ventilation, patients with status asthmaticus frequently develop severe dynamic hyperinflation, which is often associated with adverse hemodynamic effects. The development of dynamic hyperinflation can be minimized by delivering the lowest possible minute ventilation in the least possible time. Therefore, the initial ventilatory strategy should involve the delivery of relatively low tidal volumes (eg, 8-10 mL/kg) and lower respiratory rates (eg, 8-12 breaths per min) with a high inspiratory flow rate.
    • In the absence of hypoxia, hypercapnia generally is well tolerated in most patients. Even marked levels of hypercapnia are preferable to attempts to normalize the PCO₂, which could lead to dangerous levels of hyperinflation.
    • Patients often require large amounts of sedation and occasionally paralysis until the bronchoconstriction and airway inflammation have improved.
    • If a decision is made to measure trapped-gas volume (VEI), as recommended by some investigators, an attempt should be made to keep it below 20 mL/kg. The routine measurement of VEI is not recommended because measurement of plateau pressure and auto-PEEP provide similar information and are much easier to perform.
    • Patients with COPD have expiratory flow limitation and are prone to the development of dynamic hyperinflation. Here again, the goal of mechanical ventilation is to unload the respiratory muscles while minimizing the degree of hyperinflation. The use of extrinsic PEEP may be considered in spontaneously breathing patients in order to reduce the work of breathing and to facilitate triggering of the ventilator. Care must be exercised to avoid causing further hyperinflation, and the set level of PEEP should always be less than the level of auto-PEEP.
• Facilitating patient-ventilator synchrony
  • During mechanical ventilation, many patients sometimes experience asynchrony between their own spontaneous respiratory efforts and the pattern of ventilation imposed by the ventilator. This can occur with both controlled and patient-initiated modes of ventilation.
  • In order to achieve synchrony, the ventilator must not only sense and respond quickly to the onset of the patient's inspiratory efforts, it also must terminate the inspiratory phase when the patient's "respiratory clock" switches to expiration. Asynchronous interactions, commonly referred to as "fighting the ventilator," may occur when ventilator breaths and patient efforts are out of phase. This may lead to excessive work of breathing, increased respiratory muscle oxygen consumption, and decreased patient comfort.
  • Patient-ventilator asynchrony should be minimized, and a variety of ways is available to achieve this. Modern ventilators are equipped with significantly better valve characteristics compared to older-generation ventilators. Flow-triggering (with a continuous flow rate) appears to be more sensitive and more responsive to patient's spontaneous inspiratory efforts.
  • Patient-ventilator asynchrony often occurs in the presence of auto-PEEP. Auto-PEEP creates an inspiratory threshold load and thereby decreases the effective trigger sensitivity. This may be partially offset by the application of external PEEP.
  • Sometimes, additional sedation may be necessary to achieve adequate patient-ventilator synchrony.
• Noninvasive ventilatory support
  • The application of ventilatory support through a nasal or full face mask in lieu of ETT is being used increasingly for patients with acute or chronic respiratory failure.
  • Noninvasive ventilation should be considered in patients with mild-to-moderate acute respiratory failure. The patient should have an intact airway, airway-protective reflexes, and be alert enough to follow commands.
  • In clinical trials, noninvasive positive-pressure ventilation (NPPV) has proven beneficial in acute exacerbations of COPD and asthma, decompensated CHF with mild-to-moderate pulmonary edema, and pulmonary edema from hypervolemia. Reports conflict regarding its efficacy in acute hypoxemia due to other causes (eg, pneumonia). A variety of methods and systems are available for delivering noninvasive ventilatory support.
  • The benefits of NPPV depend on the underlying cause of respiratory failure. In acute exacerbations of obstructive lung disease, NPPV decreases PaCO₂ by unloading the respiratory muscles and supplementing alveolar ventilation. The results of several clinical trials support the use of NPPV in this setting.
  • In a large randomized trial comparing NPPV with a standard ICU approach, the use of NPPV was shown to reduce complications, duration of ICU stay, and mortality.⁶ In patients in whom NPPV failed, mortality rates were similar to the intubated group (25% vs 30%).
  • Plant and colleagues recently published the largest prospective randomized study comparing NPPV with standard treatment in patients with COPD exacerbation. NPPV was administered on the ward; the nurses were trained for 8 hours in the preceding 3 months. Treatment failed in significantly more patients in the control group (27% vs 15%), and in-hospital mortality rates were significantly reduced by NPPV (20% to 10%).
  • In addition, 3 Italian cohort studies with historical or matched control groups have suggested that long-term outcome of patients treated with NPPV is better than that of patients treated with medical therapy and/or endotracheal intubation.
  • In acute hypoxemic respiratory failure, NPPV also helps maintain an adequate PaO₂ until the patient improves.
  • In cardiogenic pulmonary edema, NPPV improves oxygenation, reduces work of breathing, and may increase cardiac output.
  • When applied continuously to patients with chronic ventilatory failure, NPPV provides sufficient oxygenation and/or carbon dioxide elimination to sustain life by reversing or preventing atelectasis and/or resting the respiratory muscles.
  • Patients with obesity-hypoventilation syndrome benefit from NPPV by reversal of the alveolar hypoventilation and upper airway obstruction.
  • Most studies have used NPPV as an intermittent rather than continuous mode of support. Most trials have used inspiratory pressures of 12-20 cm water; expiratory pressures of 0-6 cm water; and excluded patients with hemodynamic instability, uncontrolled arrhythmia, or a high risk of aspiration.
• Weaning from mechanical ventilation
  • Weaning or liberation from mechanical ventilation is initiated when the underlying process that necessitated ventilatory support has improved. In some patients, such as those recovering from uncomplicated major surgery or a toxic ingestion, withdrawal of ventilator support may be done without weaning. In patients who required more prolonged respiratory therapy, the process of liberating the patient from ventilatory support may take much longer.
  • A patient who has stable underlying respiratory status, adequate oxygenation (eg, PaO₂/FiO₂ >200 on PEEP <10 cm water), intact respiratory drive, and stable cardiovascular status should be considered for discontinuation of mechanical ventilation.
  • Over the years, many criteria have been used to predict success in weaning, including a minute ventilation of less than 10 L/min, maximal inspiratory pressure more than -25 cm water, vital capacity more than 10 mL/kg, absence of dyspnea, absence of paradoxical respiratory muscle activity, and agitation or tachycardia during the weaning trial. However, recent studies suggest that the rapid-shallow breathing index, ie, the patient's tidal volume (in liters) divided by the respiratory rate (breaths per min) during a period of spontaneous breathing, may be a better predictor of successful extubation. In a recent study, a daily trial of spontaneous breathing in patients with a rapid-shallow breathing index of less than 105 resulted in a shorter duration of mechanical ventilation. A spontaneous breathing trial of only 30 minutes appears adequate to identify patients in whom successful extubation is likely.
  • In patients who are not yet ready to be liberated from the ventilator, one should focus on the cause of ventilator dependency, such as excessive secretions, inadequate respiratory drive, impaired cardiac function, and ventilatory muscle weakness, rather than the type of ventilator or the mode of assistance.
  • The weaning protocol could be designed with assist-control ventilation, with gradually increasing time spent in trials of spontaneous breathing or by gradually reducing the level of PSV.
  • SIMV appears to result in less rapid weaning than PSV or trials of spontaneous breathing.
  • Patient-ventilator desynchrony is an important component in a carefully designed weaning protocol.
  • Attention must be directed toward patient comfort, avoidance of fatigue, adequate nutrition, and prevention and treatment of medical complications during the weaning period.
  • Ventilator monitoring: Peak inspiratory and plateau pressures should be assessed frequently. Attempts should be made to limit the plateau pressure to less than 25 cm water. Expiratory volume is checked initially and periodically (continuously if ventilator-capable) to assure that the set tidal volume is delivered. In patients with severe airflow obstruction, auto-PEEP (PEEPi) should be monitored on a regular basis.
• Monitoring of patients with acute respiratory failure
  • A patient with respiratory failure requires repeated assessments, which may range from bedside observations to the use of invasive monitoring.
  • These patients should be admitted to a facility where close observation can be provided. Most patients who require mechanical ventilation are critically ill; therefore, constant monitoring in a critical care setting is a must.
  • Cardiac monitoring, blood pressure, pulse oximetry, SaO₂, and capnometry are recommended. An arterial blood gas determination should be obtained 15-20 minutes after the institution of mechanical ventilation. The pulse oximetry readings direct efforts to reduce FiO₂ to a value less than 0.6, and the PaCO₂ guides adjustments of minute ventilation.
• Treatment of underlying cause
  • After the patient's hypoxemia is corrected and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place.
  • The specific treatment depends on the etiology of respiratory failure.
  • In Medication, a brief discussion of medications used to treat common causes of respiratory failure, such as cardiogenic pulmonary edema, chronic obstructive pulmonary disease, and asthma, is provided.
  • The reader is recommended to review the article specific to the disease for the workup and management of the various disorders, all of which progress by different means but ultimately converge on a final common pathway of respiratory failure.

Consultations

• Consultation with a pulmonary specialist and an intensivist are often required.
• Patients with acute respiratory failure or exacerbations of chronic respiratory failure need to be admitted to the intensive care unit for ventilatory support.

Activity

Patients generally are prescribed bed rest during early phases of respiratory failure management. However, ambulation as soon as possible helps ventilate atelectatic areas of the lung.

Medication

The pharmacotherapy of cardiogenic pulmonary edema and acute exacerbations of 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 need to be modified for some patients. Diuretics, nitrates, analgesics, and inotropics are used in the treatment of acute pulmonary edema.

Diuretics

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 IV because this allows for both superior potency and a higher peak concentration despite increased incidence of adverse effects, particularly ototoxicity.

Metolazone (Mykrox, Zaroxolyn)

Has been used as adjunctive therapy in patients initially refractory to furosemide. Has been demonstrated to be synergistic with loop diuretics in treating refractory patients and causes a greater loss of potassium. Potent loop diuretic that sometimes is used in combination with Lasix for more aggressive diuresis. Also used in patients with a degree of renal dysfunction for initiating diuresis.

Nitrates

These agents reduce myocardial oxygen demand by lowering preload and afterload. In severely hypertensive patients, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, due to 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 (Nitro-Bid, Nitrol)

SL nitroglycerin and Nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. Similar to SL, onset of Nitrospray is 1-3 min, with a half-life of 5 min. Administration of Nitrospray may be easier, and it can be stored for as long as 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients with pulmonary edema who were given Nitrospray. Topical nitrate therapy is reasonable in a patient presenting with class I-II 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, due to delayed absorption, play little role in the management of acute pulmonary edema.

Nitroprusside sodium (Nitropress)

Produces vasodilation of venous and arterial circulation. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Easily titratable.

Analgesics

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

Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to 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 desired effect is obtained.

Inotropics

Principal inotropic agents include dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In patients with hypotension presenting with CHF, dopamine and dobutamine usually are employed. Inamrinone and milrinone inhibit phosphodiesterase, resulting in an increase of intracellular cyclic AMP and alteration in calcium transport. As a result, they increase cardiac contractility and reduce vascular tone by vasodilatation.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses. Positive inotropic agent at 2-10 mcg/kg/min that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg/kg/min cause vasoconstriction, which increases afterload.

Norepinephrine (Levophed)

Used in protracted hypotension following adequate fluid replacement. Stimulates beta1- and alpha-adrenergic receptors, which in turn increases cardiac muscle contractility and heart rate, as well as vasoconstriction. As a result, 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 (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages, may cause increased heart rate, thus exacerbating myocardial ischemia. Strong inotropic agent with minimal chronotropic effect and no vasoconstriction.

Bronchodilators

These agents 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)

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

Albuterol (Proventil)

Beta-agonist useful in the treatment of bronchospasm. Selectively stimulate beta2-adrenergic receptors of the lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

Theophylline (Theo-Dur, Slo-bid, Theo-24)

Has a number of physiological effects, including increases in collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. Partially acts by inhibiting phosphodiesterase, elevating cellular cyclic AMP levels, or antagonizing adenosine receptors in the bronchi, resulting in relaxation of smooth muscle. However, clinical efficacy is controversial, especially in the acute setting.

Ipratropium bromide (Atrovent)

Anticholinergic medication that appears to inhibit vagally mediated reflexes by antagonizing 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. Dose can be combined with a beta-agonist because ipratropium may require 20 min to begin having an effect.

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 ED, they have some effect 6-8 h into therapy; therefore, early dosing is critical.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

Usually given IV in ED for initiation of corticosteroid therapy, although PO should theoretically be equally efficacious.

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• Respiratory Failure (Pediatrics: Cardiac Disease and Critical Care Medicine)
• Intraosseous Cannulation (Pediatrics: Cardiac Disease and Critical Care Medicine)
• Alveolar Proteinosis (Pediatrics: General Medicine)
• Acute Respiratory Distress Syndrome (Critical Care)

• Lung and Airway Center
• Acute Respiratory Distress Syndrome Causes
• Acute Respiratory Distress Syndrome Treatment
• Acute Respiratory Distress Syndrome Overview
• Acute Respiratory Distress Syndrome Symptoms

• Extracorporeal Membrane Oxygenation May Improve Outcomes in Severe Acute Respiratory Failure
• ECMO Can Improve Survival in Some Older Patients With Acute Respiratory Failure
• Extracorporeal Membrane Oxygenation Improves Survival in H1N1 Patients With Respiratory Failure

• Survival for Patients With HIV Admitted to the ICU Continues to Improve in the Current Era of Combination Antiretroviral Therapy
• Capnographic Monitoring of Respiratory Activity Improves Safety of Sedation for Endoscopic Cholangiopancreatography and Ultrasonography
• Positive Pressure Ventilation: What is the Real Cost?