Chapter 21. Patient with Deadly Asthma Requires Intubation

This 26-year-old man has a long history of severe asthma. His trachea has been intubated many times in the past for his asthma, most recently 2 months ago during which he spent a week in the intensive care unit (ICU). He arrives in the emergency department (ED) after an emergency medical service (EMS) transport of 15 minute during which he has been receiving continuous aerosolized salbutamol (albuterol, Ventolin) via a nebulizer. He arrives with marked respiratory distress. He is awake, diaphoretic, and is speaking in two-word sentences.

He is 5 ft 2 in (157 cm) tall and weighs 165 lb (75 kg). His vital signs are: respiratory rate (RR) 24 breaths per minute, heart rate (HR) 134 beats per minute (bpm), and blood pressure 110/60 mm Hg. His oxygen saturation is 89% on a non-rebreather and he is becoming fatigued. As he is receiving corticosteroid chronically for his asthma, he has a steroid body habitus with an edematous face and neck.

21.2.1 What Are This Patient's Vital Organ System Reserves?

Cardiovascular reserve: This is a young patient who should have adequate cardiac reserve and there should be little concern with respect to systolic and diastolic cardiac function unless there is a significant carbon dioxide retention and respiratory acidosis which would resolve with adequate ventilation. However, depending on the length of time he has been acutely ill and how adequate his oral fluid intake has been, he is likely to be volume depleted. In combination with a decrease in venous return secondary air trapping and auto-PEEP (positive end-expiratory pressure) seen with acute asthma, the presence of hypovolemia can precipitate a significant hypotension, particularly if induction agents are used to facilitate intubation. The patient has been receiving a large amount of salbutamol, a medication with significant β1-agonist properties. In combination with stress and hypercapnia, there is a significant arrhythmia potential from large amounts of salbutamol. Depending on how much β1-agonist he has been taking, there is a high likelihood that he is also relatively hypokalemic due to the cellular shifting of potassium caused by the β1-agonist. This may contribute to the potential for arrhythmia as well. When choosing induction agents for this patient, it is important to keep in mind that they all have negative inoptropic properties.

CNS reserve: There is nothing to indicate that this patient will respond abnormally to standard doses of induction agents, keeping in mind that he is obese and should be dosed accordingly. However, the practitioner ought to be watchful for agitation, confusion, or somnolence associated with carbon dioxide retention, in which case sensitivity to sedative hypnotic induction agents ought to be anticipated. Respiratory acidosis can potentiate myocardial depression associated with anesthesia induction agents.

Respiratory reserve: Patients with severe asthma have prolonged expiratory phases and air trapping.1 Tidal volume is limited, with minimal or no respiratory reserve. Intubation may be indicated as these patients can become significantly fatigued and as such, are unable to maintain gas exchange on their own. Substantial ventilation-perfusion mismatch is present, which limits the ability to oxygenate and denitrogenate the lungs prior to induction. Preinduction hypoxemia will rapidly ensue following the administration of paralytics or induction agents.

21.3.1 Employing the Mnemonics Suggested in Chapter 1, Is This a Difficult Airway?

Yes! Facial and neck edema from chronic steroid dependence may make bag-mask-ventilation (BMV) difficult. In addition, this patient is obese and in status asthmaticus, both of which are associated with very high airway pressures that can be difficult or impossible to overcome with a positive-pressure BMV. Other than these factors, there appear to be no other predictors of a difficult BMV when applying the mnemonics MOANS (see Section 1.6.1).

Using the LEMON airway evaluation (see Section 1.6.2), the neck and face edema may make laryngoscopy difficult. As he has experienced many tracheal intubations in the past, in conjunction with corticosteroids and mechanical ventilation, subglottic stenosis is a possibility that must be considered. However, the geometry of his upper airway appears normal, and he has a Mallampati Class II airway. His neck appears to be freely mobile.

A recommended mnemonic to assist the assessment of the feasibility of using an extraglottic device (EGDs) is RODS (see Section 1.6.3). Restricted mouth opening is not an issue in this patient and upper airway obstruction is only a possibility. However, he has severe obstructive respiratory disease and his compromised pulmonary compliance, the "stiffness of the lungs," will seriously limit usefulness of an EGD just as BMV may be difficult.

While there are only a few indicators of a potentially difficult airway, he may not be an optimal candidate for a rapid-sequence intubation (RSI). A failed intubation in a hypoxemic person with very poor lung compliance would be a very dangerous situation. On the other hand, there is no reason to believe that a surgical airway would be difficult in this patient (SHORT, see Section 1.6.4). The decision to perform RSI should be in the context of the experience of the practitioner as well as the device(s) being used and availability of backup. For instance, the use of RSI may be very different if the practitioner is using a video laryngoscope instead of a standard laryngoscope.

21.3.2 Are There Any Other Airway Concerns in a Patient with Status Asthmaticus?

This patient has no respiratory reserves, rapid oxygen desaturation, hypotension, and possible subglottic stenosis. The insertion of a tracheal tube in a person who is already in bronchospasm may exacerbate his condition.

21.3.3 Have We Medically Optimized His Treatment Prior to Tracheal Intubation?

For reasons already outlined, avoiding intubation would be the best option if at all possible. β2-Agonists are the mainstay of treatment in asthma.2 However, this patient has been on continuous bronchodilators for the 15-minute transport and had utilized his inhaler every 15 minutes at home prior to calling the paramedics. The addition of corticosteroid may be beneficial for this patient with an acute exacerbation of asthma,3 although the delayed onset of action for corticosteroids will not be helpful in avoiding intubation in the immediate/emergent period.

21.3.4 What Additional Therapies Are Available to This Patient?

Anticholinergics: Meta-analysis suggests that there is a modest benefit in adding this therapy to β2-Agonists.4 The benefits appear to outweigh the potential risks for the patient, so anticholinergics should be considered in this case.

Magnesium: Two meta-analysis have been performed analyzing the effect of IV magnesium on patients with asthma.5,6 Seven trials were identified and the investigators conclude that magnesium has no confirmed role in the management of mild or moderate asthma. In severe asthma, there is evidence that magnesium improves pulmonary function and hospitalization rates, although there is no good evidence that in severe asthma magnesium decreases the need for intubation. Magnesium is unlikely to cause harm. However administration should not delay intubation or any other therapy.

Noninvasive ventilatory support (NIVS): One randomized trial and several small uncontrolled trials support the use of NIVS in acute asthma.7 NIVS has been demonstrated to improve expiratory flow rates and reduce the need for hospitalization, although a recent meta-analysis by Ram et al concluded that routine use of NIVS in severe acute asthma could not be recommended.8

21.3.5 What Are the Possible Options Regarding Airway Management in This Patient?

In this particular patient, and despite the reservations that have been mentioned, RSI by a skilled practitioner is probably the best choice. Planning ahead is crucial, as is deciding on a Plan B and C in the event Plan A should fail. While recognizing the limitations of denitrogenation prior to tracheal intubation (described earlier), the practitioner ought to administer as high an oxygen concentration as possible to the patient, employing a bag-mask unit if the patient can tolerate its use. As an added advantage, the practitioner can provide gentle assisted ventilation to the patient if he is able to tolerate it, taking care not to cause insufflation of the stomach, vomiting, or gagging. Rapid-sequence induction drugs chosen should be administered to the patient while he remains in a comfortable position, in this patient most commonly sitting upright. Once the patient loses consciousness, the patient can be placed in the supine position and laryngoscopy and intubation performed. A large, 8.0 mm ID or larger, endotracheal tube is preferred in order to reduce resistance and facilitate aggressive pulmonary toilet.

If time permits, patients with reactive airway disease or obstructive lung disease should be administered with 1.5 mg·kg−1 of IV lidocaine 3 minutes before tracheal intubation in order to attenuate the reflex bronchospasm in response to airway manipulation, which is thought to be mediated via the vagus nerve.9-11 The recommendation to use IV lidocaine in RSI protocols for the severe asthmatic is extrapolated from the results of studies employing healthy volunteers with a history of bronchospastic disease.12-14 Unfortunately, there is also evidence that IV lidocaine does not protect against intubation-induced bronchoconstriction in asthma. In a prospective, randomized, double-blind, placebo-controlled trial of 60 patients, lidocaine and placebo groups were not different in their transpulmonary pressure and airflow immediately after intubation and at 5-minute intervals.15 Until more data are available, it seems reasonable to minimize the risk of intubation-induced bronchoconstriction by using lidocaine premedication in the asthmatic if time and resources permit.

Ketamine is generally considered to be the induction agent of choice in the asthmatic patient because it increases circulating catecholamines and inhibits vagal outflow. In addition, it is a direct smooth muscle dilator and it does not cause histamine release.16 While case reports of dramatic improvement in pulmonary function with ketamine have driven its popularity,17,18 no randomized studies have been performed to demonstrate ketamine's superiority over other agents. In a case series, 19 of 22 asthmatic patients with active wheezing had a decrease in bronchospasm during ketamine-induced anesthesia.19 In one prospective, placebo-controlled, double-blind trial of 14 mechanically ventilated patients with bronchospasm, the 7 patients treated with 1.0 mg·kg−1 ketamine had a significant improvement in oxygenation but no improvement in PCO2 or lung compliance. In addition, the outcome (discharge from the ICU) was the same in both groups. The study population was heterogeneous, making conclusions of the benefit of ketamine difficult at best.20 A randomized, double-blind, placebo-controlled trial of low-dose IV ketamine, 0.2 mg·kg−1 bolus followed by an infusion of 0.5 mg·kg−1·hour−1, in nonintubated patients with acute asthma failed to demonstrate a benefit in IV ketamine.21

Although evidence is limited, at the present time, based on its mechanism of action and safety profile, ketamine appears to be the best agent available for RSI in the asthmatic. Intravenous ketamine 1.5 mg·kg−1 should be given immediately before the administration of 1.5 mg·kg−1 of succinylcholine.

21.3.6 How Would You Intubate the Trachea of This Patient?

1. Preprocedure preparations:

   The following difficult airway devices should be ready if available:

   • An Eschmann Introducer (gum-elastic bougie)
   • A fiberoptic or video laryngoscope if available
   • A cricothyrotomy kit
   • An intubating LMA™

   The following drugs should be available:

   • Lidocaine at 1.5 mg·kg−1 IV in syringes
   • Ketamine at 1 to 2 mg·kg−1 in syringes
   • Succinylcholine at 1.5 to 2 mg·kg−1 in prefilled syringes
   • Sedation and paralytic agents for postintubation management

2. Cardiac monitors are applied along with pulse oximetry. Denitrogenation is achieved using high-flow oxygen with the patient sitting.

3. Lidocaine is administered IV at 1.5 mg·kg−1. This should be given about 3 to 5 minutes prior to the actual laryngoscopy if time and resources permit.

4. Ketamine is administered IV and the patient is observed until unconscious. This should take 1 to 2 minutes.

5. Succinylcholine is administered. The patient is placed supine with the head and neck placed in a sniffing position. Cricoid pressure is applied if not contraindicated. The patient is observed for fasiculations.

6. Laryngoscopy is performed. The cords are visualized easily and the endotracheal tube (ETT) is passed and secured.

7. Capnography is used to confirm correct tracheal placement.

8. Postintubation drugs are administered for sedation and paralysis.

21.4.1 What Are the Appropriate Ventilator Settings for This Patient Following Tracheal Intubation?

All asthmatic patients have obstructed small airways and dynamic alveolar hyperinflation with varying amounts of end-expiratory residual intra-alveolar gas and pressure (auto-PEEP or intrinsic PEEP). Elevations in auto-PEEP increase the risk for baro/volutrauma. Reversal of airflow obstruction and decompression of end-expiratory filled alveoli are the primary goals of early mechanical ventilation in the asthmatic. The former requires continuous in-line nebulization with increasingly higher doses of β2-agonists until reversal is objectively measured (decrease in peak and plateau airway pressures) or unacceptable side effects are produced. Safe, uncomplicated alveolar decompression requires a prolonged expiratory time (I:E of 1:4 to 1:5). This is achieved by using smaller tidal volumes than usual, with a high inspiratory flow (IF) rate to shorten the inspiratory cycle time, permitting a longer expiratory phase.22

The initial goal of ventilator therapy in the asthmatic patient is to improve arterial oxygen tension to adequate levels without inflicting barotraumas on the lungs or increasing auto-PEEP. Initial tidal volume should be reduced as necessary, to avoid barotrauma and air trapping. The speed at which a mechanical breath is delivered in liters per minute, typically 60 L·min−1, is called the IF rate. In asthma, the initial IF should be increased to 80 to 100 L·min−1 with a decelerating flow pattern. A pressure control paradigm is preferred over volume control. If volume control is chosen, the ideal waveform is one of deceleration rather than constant (square). The ventilation rate should be relatively low in order to allow sufficient time for alveolar decompression. It is acceptable to permit the maintenance or gradual development of hypercapnia through reduced minute ventilation, as this reduces the potential for barotrauma. High intrathoracic pressure caused by air trapping may compromise cardiac output and produce hypotension and therefore should be avoided.23,24

The highest measured pressure at peak inspiration is the peak inspiratory pressure (PIP). The compliance of the lungs, chest wall, ventilatory circuit, and ventilator; the resistance of the ETT; and the effect of mucous plugs all contribute to the PIP. This reading has an inconsistent predictive value for baro/volutrauma but ideally should be kept under 50 cm H2O. A sudden rise in PIP should be interpreted as indicating tube blockage, mucus plugging, or pneumothorax until proven otherwise. A sudden, dramatic fall in PIP may indicate extubation.

The measured intra-alveolar pressure during a 2 to 4 second end inspiratory pause is referred to as the plateau pressure (Pplat). Values less than 30 cm H2O are best and are not usually associated with baro/volutrauma. Measurement and trending of Pplat are excellent objective tools to confirm optimal ventilator settings and the patient's response as well as the reversal of airflow obstruction. If initial ventilator settings disclose a Pplat of more than 30 cm H2O, consider lowering minute ventilation and increasing IF, both of which will prolong expiratory time and attenuate hyperinflation. If Pplat is unavailable, PIP may be used as a surrogate.

Most patients in status asthmaticus who require intubation are initially hypercapnic. The concept of controlled hypoventilation (permissive hypercapnia) promotes gradual development (over 3-4 hours) and maintenance of hypercapnia (PCO2 up to 90 mm Hg) and acidemia (pH as low as 7.2). This is done primarily to decrease the risk of ventilator-related lung injury and prevent hemodynamic compromise as a result of increasing intrathoracic pressure from auto-PEEP or intrinsic PEEP (PEEPi). Permissive hypercapnia is usually accomplished by reducing minute ventilation, increasing IF rate to 80 to 120 L·min−1, and paralyzing and heavily sedating (usually paralyzing) patients who otherwise would not tolerate these settings. Permissive hypercapnia may be instrumental in promoting prolonged expiratory times and reducing auto-PEEP.25

21.4.2 What Are the Initial Ventilator Settings for This Patient?

1. Determine the patient's ideal body weight.

2. Set a tidal volume of 6 to 8 mL·kg−1 with an FiO2 of 1.0 (100% oxygen).

3. Set a respiratory rate of 8 to 10 breaths per minute.

4. Set an inspiratory to expiratory ratio of 1:4 to 1:5. Pressure control is preferred. If using the pressure control, the I:E ratio is adjusted directly by the I:E ratio parameter, or by adjusting the inspiratory time parameter. If using volume control, the I:E ratio can be adjusted by increasing the peak flow rate, and the "ramp" inspiratory waveform should be selected. Peak IF can be as high as 80 to 100 L·min−1.

5. Measure and maintain the plateau pressure at less than 30 cm H2O or try to keep PIP at less than 50 cm H2O.

6. Focus on the oxygenation and pulmonary pressures initially. If necessary, allow maintenance or gradual development of hypercapnia to avoid high plateau pressures and increasing auto-PEEP.

7. Assure continuous sedation with a benzodiazepine and paralysis with a nondepolarizing muscle relaxant. The practitioner may consider a continuous ketamine infusion for sedation and potential smooth muscle relaxation.

8. Continue in-line β2-agonist therapy and additional pharmacologic adjunctive treatment based on the severity of the patient's illness and objective response to treatment.

The patient with severe asthma constitutes a difficult airway even without features that might predict difficult laryngoscopy and intubation due to the fact that BMV and EGD rescue is likely to be difficult or impossible. A cuffed endotracheal tube in the trachea is essential to permit adequate positive pressure ventilation, and this suggests that rescue techniques, such as employing noncuffed tracheal devices, transtracheal jet ventilation, noncuffed Seldinger cricothyrotomy devices, and so on are of little use.

If the use of medications to facilitate intubation is contemplating, the practitioner should consider lidocaine and ketamine. A continuous infusion of ketamine may be of use following intubation. Postintubation hypotension ought to be expected and managed aggressively with fluids and vasopressor if indicated, recognizing tension pneumothorax as a cause of precipitous hemodynamic change. Ventilation strategies ought to include low volumes and respiratory rates with long expiratory times and slow peak IF rates. Arterial carbon dioxide levels are not of immediate concern, provided the arterial pH can be maintained at a level consistent with reasonable cardiac, liver, and renal function.