Common misconceptions and mistakes
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Labeling a patient as “failure to wean” because of a rapid shallow breathing pattern (ie, increased rapid shallow breathing index [RSBI]) during spontaneous breathing trial (SBT) despite persistently alkalotic blood gasses
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Labeling a volume overloaded patient as ventilator dependent
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Allowing an awake patient to fail an SBT because of “apnea”
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Accepting agitation and/or adrenergic signs of distress (ie, increased heart rate [HR], increased blood pressure [BP]) as the reason for failing an SBT, without obtaining an arterial blood gas (ABG) test to see if these were caused by respiratory failure or delirium
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Forgetting to consider suctioning frequency (secretion burden) while considering readiness to extubate
Approach to extubation
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Background:
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Each day on the ventilator increases the risk of ventilator associated pneumonia (VAP)
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VAP increases intensive care unit (ICU) mortality; therefore:
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Must extubate people as soon as they are ready to prevent unnecessary morbidity and mortality
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May err on the side of extubating “early,” accepting (up to) a 10% reintubation rate, in attempts to avoid keeping people on the ventilator longer than necessary
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Liberation versus weaning
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The classical approach to extubation involved “weaning”:
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Incrementally withdrawing support, over time, on the assumption that muscle retraining is required for most patients, after experiencing the muscle “rest” of complete ventilator support
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This concept is not supported by diaphragmatic muscle physiology and places patients at risk for being on the ventilator longer than necessary (increasing VAP risk)
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Liberation (the modern approach) assumes that an individual should be ready to breathe spontaneously again when the original insult requiring intubation has resolved; no training required (assuming no significant injury to lung function occurred during the acute illness)
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A “liberation” approach to extubation involves observing a patient for 30–120 minutes during an SBT
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Spontaneous breathing means that, despite connection to the ventilator circuit, no significant ventilatory support is given
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Any and all airway pressure added to the circuit is done to provide physiologic PEEP and to overcome resistance in the system imparted by the tubing
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Patients are observed for the development of rapid shallow breathing (panting), a physical pattern associated with diaphragmatic fatigue, and hypercapnic respiratory failure
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This diaphragmatic fatigue pattern can be quantified by the RSBI, which equals the respiratory rate divided by tidal volume:
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Yang and Tobin et al. (Determining readiness for liberation after a SBT, NEJM 1991;324(21):1445-1450) showed that the RSBI after 30 minutes of spontaneous breathing could predict the success or failure of subsequent extubation (negative predictive value > positive predictive value):
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An RSBI ≤ 105 predicted successful extubation 78% of the time (positive predictive value)
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An RSBI > 105 predicted failure 95% of the time (negative predictive value)
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The contemporary approach to extubation is to “liberate patients” after a successful spontaneous breathing trial, defined as an RSBI ≤ 105 after at least 30 minutes of spontaneous breathing
Assessing readiness to extubate ( Fig. 1 )
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All intubated patients should be assessed daily for their readiness to be extubated by asking three questions.
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Question 1: Has the original insult requiring intubation (eg, septic shock, volume overload) significantly improved or resolved?
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This is a subjective determination that the event or catastrophe necessitating intubation has improved enough to consider a spontaneous breathing trial (typically after the first 24 hours of critical care)
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Question 2: Does the patient require minimal oxygenation, ventilation, and endotracheal (ET) tube support?
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Oxygenation support is determined by the Fi o 2 and the positive end-expiratory pressure (PEEP) required to maintain a Pa o 2 > 60 mm Hg
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The Fi o 2 should be low enough that it can be reliably delivered non-invasively (typically ≤ 50%)
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The PEEP should be ≤ 5 cm H 2 O (ie, physiologic)
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Ventilatory support is determined by the minute ventilation required to achieve a normal p
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Minimal ventilatory support implies that a normal minute ventilation (ie, 5–10 L/min) will yield a normal pH (7.35–7.45)
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Patients with an elevated minute ventilation (MV) either have increased ventilatory needs (evidenced by a pH < 7.40) or are hyperventilating (evidenced by a pH ≥ 7.40)
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Acidotic patients (pH < 7.4) with an elevated MV and a P co 2 < 40 mm Hg are compensating for metabolic acidosis
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Acidotic patients (pH < 7.4) with an elevated MV and a PCO 2 ≥ 40 mm Hg are compensating for increased dead space (as occurs in pulmonary embolism) or increased CO 2 production (as occurs in fever)
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Either way, this increases their risk for diaphragmatic fatigue (and hypercapnic failure), and should prompt consideration for:
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Replacing base deficit in individuals with renal failure as the cause of their metabolic acidosis (common)
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Keeping the patient intubated until lactate and/or ketones clear
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Keeping the patient intubated until dead space and/or CO 2 production decreases
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Even if the patient does well after 120 minutes of spontaneous breathing, consider increasing the SBT time by an additional 2–6 hours to ensure adequate stamina
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Alkalotic patients (pH > 7.4) with an elevated MV are hyperventilating, implying agitation, anxiety, or a respiratory rate set too high
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These patients should be considered for an SBT, and extubation if successful
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Anticipate initial SBT intolerance secondary to apnea (given alkalosis and its inhibitory effect on ventilation)
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If the patient is overbreathing the ventilator despite sedation, anticipate delirium and consider treating with either:
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Haloperidol (all other neuroleptics are sedating)
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Dexmedetomidine (much faster but much less reliable)
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ET tube support (suctioning needs and upper airway patency)
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Always check with respiratory therapy and/or nursing regarding the frequency of the patienťs suctioning requirements
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Q1–2-hour suctioning requirements (ie, copious respiratory secretions) make successful extubation difficult
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Copious pulmonary secretions should be presumed to be infectious, requiring culture, empiric antibiotics, and chest physiotherapy
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The above interventions usual take 24–48 hours before secretions improve and extubation can be reconsidered
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Upper airway patency:
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The ET tube may mask upper airway narrowing caused by laryngeal edema or extrinsic compression
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To ensure upper airway patency, always check for an audible expiratory “cuff leak” prior to extubation:
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Deflate the ET tube cuff
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Deliver a breath
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Listen for air flowing through the upper airway as the breath escapes the trachea by traveling up, through the vocal cords, and around the ET tube, (suggesting a patent upper airway)
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The cuff leak is often audible at the bedside without a stethoscope
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Occasionally a stethoscope, positioned high in the neck, is required
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The cuff leak should be very loud via stethoscope
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The lack of an audible expiratory “cuff leak” raises concern for upper airway narrowing and/or laryngeal edema (see evaluation below)
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Question 3: Does the patient tolerate 30–120 minutes of spontaneous breathing? (There is only one way to find out.)
Performing an SBT
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Turn off sedation
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Reduce pain medication to the minimal effective dose
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Change the ventilator to a pressure support mode (no mandatory breaths)
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Set pressure support and PEEP:
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Pressure support should be minimal (0–5 cm H 2 O) to overcome resistance in the tubing
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The smaller the ET tube, relative to the size of the person (eg, #6 tube in a 6″ male), the higher the pressure support
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Physiologic PEEP is used (5 cm H 2 O)
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The patient is observed for 3 minutes, screening for initial intolerance (ie, immediate failure), too quick to reflect respiratory failure secondary to abnormal pulmonary mechanics or function
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Initial intolerance (< 3min) is typically caused by delirium, pain, or persistent sedative effect
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Diagnosis hinges on directly observing and interacting with the patient during the spontaneous breathing attempt
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Apnea, the most common reason for initial SBT intolerance, occurs in either awake or sleeping patients
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“Awake Apnea” is almost always secondary to the patient being alkalotic at the start of the SBT (often evident on the morning of ABG)
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However, the respiratory alkalosis may occur just prior to the SBT, when sedation and pain medication are stopped/weaned
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The patient should be given more time to allow CO 2 to rise and pH to fall (the normal stimulus for ventilation)
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Though often unnecessary, the patient can be preoxygenated to ensure desaturation will not occur
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“Sleeping Apnea” implies oversedation (± narcotic effect) and is managed by waiting more time, decreasing narcotics, and then reattempting an SBT
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Ineffective respirations are the next most common cause of initial SBT intolerance, occurring with either agitation or sleepiness
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Agitation, in this context, implies delirium and should be treated with either haloperidol or dexmedetomidine (as described below)
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Sleepiness, in this context implies persistent sedative effect, and patients should be given more time to wake up before repeat SBT
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Signs of adrenergic distress (increased HR and BP):
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Tachycardia and hypertension occur in agitated individuals and may represent pain or delirium, occurring as sedation and analgesia are weaned, in preparation for the SBT
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Agitated patients on mechanical ventilation should always be queried about pain
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When pain is endorsed, narcotic dosing should be increased
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The SBT can be reattempted when pain is better controlled
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If the patient demonstrates initial SBT tolerance, he or she should be observed for 30–120 minutes and screened for the development of a pathologic rapid shallow breathing pattern indicative of diaphragmatic fatigue and impending hypercapnic respiratory failure (ie, an RSBI > 105)
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If the patient does well for 30–120 min, then consider extubation (no ABG required), specifically if the following are true of the patient:
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RSBI < 105
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Awake and following commands
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Denies dyspnea
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Audible cuff leak
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Yang and Tobin’s data also show that requiring patients to spontaneously breath for 2 hours instead of 30 minutes does not identify additional extubation failures, such that 30 minutes is considered an adequate time interval for evaluation
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That said, one should have a very low threshold to increase SBT time to test stamina
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This is especially crucial in patients with neuromuscular weakness, who are prone to delayed fatigue and failure
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Patients with cardiogenic pulmonary edema may gain significant support from very low pressures (ie, PEEP of 5 cm H 2 O) such that they often warrant an additional SBT challenge, specifically zero PEEP
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A zero end-expiratory pressure (ZEEP) trial ensures that patients will not develop worse alveolar edema with extubation
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As always, patients should be trialed for 30–120 minutes
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The higher the concern for failure, the longer the SBT
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Troubleshooting apparent sbt failure ( Fig. 2 )
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Failure should be characterized as either:
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High RSBI (f/TV ratio > 105)
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Signs of systemic adrenergic distress (elevated HR and BP)
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Agitation
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Dyspnea
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Oxygen desaturation (unusual), implying V/Q mismatch occurring during spontaneous breathing (requires separate consideration)
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Patients demonstrating a RSBI > 105 , adrenergic distress, agitation, and/or complaints of dyspnea after 30–120 minutes of spontaneous breathing need an overall subjective assessment of whether the failure was anticipated
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Anticipated failure occurs when individuals, despite improvement, are still suffering from acutely abnormal pulmonary mechanics/function
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Unanticipated failure occurs when the reason for intubation has resolved (eg, surgical procedure) and pulmonary mechanics/function are near baseline
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Anticipated failure needs no further workup:
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Patients should be placed back on mechanical ventilation
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The patient may do more spontaneous breathing later in the day, for “exercise,” but the general practice is to optimize pulmonary mechanics for next 24 hours, before a repeat extubation assessment/attempt
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Yang and Tobin’s data also showed no difference in detecting the ability to extubate patients, when comparing once daily SBTs to multiple SBTs throughout the day (hence the rationale for 24 hours of optimization before trying again)
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Unanticipated SBT failure should be evaluated with an ABG (obtained before return to mechanical ventilation)
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Patients with a respiratory alkalosis (pH > 7.40, P co 2 < 40 mm) may be delirious and/or encephalopathic, but are not in respiratory failure (despite their breathing pattern or subjective complaints)
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A respiratory alkalosis (not driven by hypoxemia) proves respiratory reserve and will not cause diaphragmatic fatigue
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Extubation should be considered, in those who can follow commands, and may resolve the delirium, agitation, and dyspnea (by restoring upper airway airflow sensation)
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Patients with an acidotic pH, in the normal range (ie, 7.35–7.39) may be delirious or encephalopathic (ie, respiratory failure is not the explanation for their breathing pattern, agitation, or distress), or they may be in respiratory failure, developing acute hypercapnia at the time the ABG was drawn
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These patients should be observed for an additional 2–6 hours of spontaneous breathing, before having their ABG repeated:
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A repeat ABG showing that the pH has remained normal is very reassuring, and extubation should be considered
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A repeat ABG showing that the pH has fallen to < 7.35 and the P co 2 has increased > 40 mm Hg is very concerning for the development of diaphragmatic fatigue, requiring return to mechanical ventilation
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Patients with a metabolic acidosis and complete compensation (ie, pH < 7.35, P co 2 < 35 mm Hg) should be observed for an additional 2–6 hours of spontaneous breathing, before having their ABG repeated, to ensure that they can maintain the elevated MV required by the acidosis
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A repeat ABG showing continued appropriate compensation is reassuring, and extubation should be considered
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Patients with a metabolic acidosis and partial compensation (ie, pH < 7.35, P co 2 < 40 mm Hg) should be observed for an additional 2–6 hours of spontaneous breathing, before having their ABG repeated, to ensure that the partial compensation is not a sign of diaphragmatic fatigue, but rather blunted ventilatory drive
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A repeat ABG showing a stable P co 2 < 40 is reassuring
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Consider increasing the length of the SBT versus a trial of extubation
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Consider replacing base deficit in individuals with renal failure as the cause of their metabolic acidosis
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Patients with an acute respiratory acidosis (ie, pH < 7.35, P co 2 > 40 mm Hg) have objectively failed their spontaneous breathing trial and should be returned to mechanical ventilation
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Because failure was unanticipated, an evaluation of lung mechanics is warranted (ie, physical exam, chest x-ray [CXR], peak and plateau pressure assessment when back on volume-controlled [VC] ventilation)
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SBT failure secondary to oxygen desaturation:
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At the point patients are considered ready for a SBT, they should require minimal oxygenation support (ie, FIO 2 ≤ 50%, PEEP ≤ 5 cm H 2 O)
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This implies reasonably appropriate V/Q matching
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Even when patients develop hypercapnic respiratory failure on an SBT, desaturation is not expected (because of supplemental oxygen)
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Hypoxemia from hypoventilation requires a normal FIO 2 (ie, 21%)
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Providing an FiO 2 ≥ 40% will prevent hypoventilation-mediated hypoxemia
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The act of spontaneous breathing should not change V/Q relationships significantly, such that sudden hypoxemia during an SBT is an unusual event with a limited differential (ie, flash pulmonary edema, mucus plugging, bronchospasm)
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Ischemia and flash pulmonary edema, are suggested by:
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Crackles and/or copious pink, thin, frothy secretions on physical exam
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Elevated peak and plateau pressures when placed back on VC
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Interstitial and/or alveolar edema on CXR
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Elevated cardiac markers or ischemic electrocardiogram (ECG) changes
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Occasionally patients with severe coronary artery disease (CAD) require cardiac intervention prior to liberation
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Mucus plugging and lung collapse are suggested by:
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Focally decreased breath sounds and/or copious thick secretions on physical exam
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Elevated peak airway pressures with a peak to plateau pressure difference > 15
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Segmental or subsegmental collapse on CXR
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Bronchospasm is suggested by
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Wheezing on physical exam
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Elevated peak airway pressures with a peak to plateau pressure difference > 15
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Sudden bronchospasm, in an individual without known obstructive lung disease, usually represents cardiac asthma (ie, a manifestation of flash pulmonary edema) or drug allergy
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