Part 8: Advanced Challenges in ResuscitationSection 3: Special Challenges in ECC

3C: Near-Fatal Asthma

Introduction

This section of the International Guidelines 2000 focuses

on near-fatal asthma. The recommendations deviate imme-

diately from routine asthma care and address the sequence

of action steps needed to prevent death. Some recommenda-

tions, such as use of aminophylline, permissive hypercarbia,

and early tracheal intubation, do not re¯ect routine asthma

attacks. Nevertheless, in the desperate race to prevent cardi-

opulmonary arrest, heroic measures must be considered and

considered early.

Severe exacerbation of asthma can lead to several forms

of sudden death. One classi®cation scheme categorizes

asthma on the basis of the onset of symptoms. Signs of

rapid-onset asthma develop in ,2.5 hours, signs and symp-

toms of slow-onset asthma develop over several days [1].

Cardiac arrest in patients with severe asthma has been

linked to

² Severe bronchospasm and mucous plugging leading to

asphyxia [2] (this condition causes the vast majority of

asthma-related deaths).

² Cardiac arrhythmias due to hypoxia, which is the

common cause of asthma-related arrhythmia. In addition,

arrhythmias are caused by use of b-adrenergic agonists.

(In rare instances these arrhythmias may be due to

prolongation of the QT interval resulting from b-adrener-

gic agonists [3±5] or toxicity caused by medications such

as theophylline.)

² Auto-PEEP (positive end-expiratory pressure) occurs in

some patients who are intubated and mechanically venti-

lated. Patients fail to expire as much air as they took in;

gradual buildup of pressure occurs and reduces blood

¯ow and blood pressure. Auto-PEEP is secondary to air

trapping and `breath stacking' (breathed air entering and

being unable to escape).

² Tension pneumothorax (often bilateral)

Most asthma-related deaths occur outside the hospital.

The number of patients with severe attacks of asthma who

present to the Emergency Department at night is 10 times

greater than the number presenting during the day [6].

Multiple factors affect the outcome of therapy in asthmatic

patients. Constantly review these issues during evaluation

and treatment:

² Determine whether the patient has true acute asthma.

When a patient presents with dyspnea in extremis you

may not be able to obtain the recent history.

² Depending on the patient's history and medication use,

other conditions may be present. These include

±Cardiac disease (congestive heart failure, myocardi-

tis), pulmonary disease (emphysema, pneumonia,

upper-airway obstruction±structural or psychogenic),

acute allergic bronchospasm or anaphylaxis (aspirin,

foods, or idiopathic), pulmonary embolism, or vascu-

litis (Churg-Strauss syndrome) [7].

±Medications and drugs of abuse: bronchospasm as

sequelae to medications (b-blockers) [8] or drugs of

abuse (cocaine and opiates) [9,10].

±Discontinuation of corticosteroids. Patients who have

used corticosteroids for a long time may have relative

adrenal insuf®ciency. With the stress of discontinua-

tion of the steroids and the adrenal insuf®ciency, these

patients may present with near-fatal asthma.

Key Interventions to Prevent Arrest

The major clinical action is to treat the severe asthmatic

crisis aggressively, before deterioration to full arrest. The

speci®c agents and the treatment sequence will vary accord-

ing to local practice. Emergency treatment will include

some combination of the agents and interventions discussed

below. The challenge of most concern for the ALS provider

is the patient who deteriorates progressively, unresponsive

to multiple therapeutic efforts.

Oxygen

Use a concentration of inspired oxygen to achieve a Pao2

of $92 mm Hg. High-¯ow oxygen by mask is sometimes

necessary. In patients with an asthmatic crisis, the following

signs indicate that the need for rapid tracheal intubation is

imminent:

² Findings of obtundation

Resuscitation 46 (2000) 279±283

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www.elsevier.com/locate/resuscitation

² Profuse diaphoresis

² Poor (`¯oppy') muscle tone (clinical signs of hypercar-

bia)

² Findings of severe agitation, confusion, and ®ghting

against the oxygen mask (clinical signs of hypoxemia)

[11]

² Elevation of the Pco2 by itself is not indicative of a need

for tracheal intubation. Elevated Pco2 does indicate

severity of the episode. Reserve intubation for patients

with the clinical ®ndings mentioned above or a clearly

rising Pco2. Treat the patient, not the numbers.

Nebulized b 2-Agonists

Albuterol (salbutamol) is the cornerstone of therapy for

acute asthma in most of the world. Standard practice in

Emergency Departments is a dose of 2.5 to 5.0 mg every

15 to 20 minutes given up to 3 times in 1 hour (total dose of

7.5 to 15 mg/h). Patients who do not respond to albuterol

may respond well to subcutaneous epinephrine or terbuta-

line [12].

Intravenous Corticosteroids

By 2000 it became a common practice in accident and

emergency departments to begin corticosteroid therapy

early (in the ®rst 30 minutes) for patients with life-threaten-

ing asthma. Corticosteroids should be started early, but

oxygen and b-agonists always have priority as the initial

agents. Clinicians typically use 125 mg of methylpredniso-

lone (or equivalent hydrocortisone 200 mg IV) as a starting

dose in cases of severe asthma [13±15]. Doses can range as

low as 40 mg to as high as 250 mg IV or its equivalent.

Nebulized Anticholinergics

Use ipratropium, an inhaled anticholinergic agent, as a

moist nebulizing agent in combination with albuterol at a

dose of 0.5 mg [16]. Unlike b2-agonists, which have an

immediate onset of action, nebulized anticholinergic agents

have a delayed onset of approximately 20 minutes.

Intravenous Aminophylline

Aminophylline, now used as secondary therapy after b2-

agonists and corticosteroids, can enhance the effects of

those agents. As a bronchodilator aminophylline is approxi-

mately one third as potent as b2-agonists. Clinicians use

aminophylline much more frequently in children than in

adults. A loading dose of 5 mg/kg is given over 30 to 45

minutes followed by an infusion of 0.5 to 0.7 mg/kg per

hour, but this loading dose is not advised in people already

taking theophylline, who should receive either half loading

doses or maintenance doses. Addition of this agent to high

doses of b2-agonists is thought to increase side effects more

than it increases bronchodilation. This is most evident in

patients already taking theophyllines. The risk-bene®t

ratio may be different in patients not taking theophyllines

[17].

Intravenous Magnesium Sulfate

A number of authors have reported success with magne-

sium sulfate in patients refractory to inhaled adrenergic

agents and corticosteroids. Although not consistently effec-

tive, magnesium is widely available and can be adminis-

tered with few if any side effects at a dose of 2 to 3 g IV

at rates as fast as 1 g/min (1 g magnesium sulfate� 98 mg of

elemental magnesium) [18,19].

Parenteral or Subcutaneous or Intramuscular Epinephrine

or Terbutaline

Subcutaneous administration of epinephrine or terbuta-

line may prevent the need for arti®cial ventilation in cases

of life-threatening asthma, especially in patients who do not

respond to inhaled b2-agonists. The total epinephrine dose

(at a concentration of 1:1000) is 0.01 mg/kg, usually divided

into 3 doses at 20-minute intervals. For convenience and

easy recall a non-weight-based dose of 0.3 mg usually is

given to adults. This dose of epinephrine (0.3 mg) can be

repeated twice at 20-minute intervals to a total of 3 injec-

tions.

The dose of terbutaline is 0.25 mg SC every 30 minutes;

up to 3 doses may be given. At this time there is no good

evidence of advantages for IV b-agonists over inhaled

bronchodilators.[20] The value of IV bronchodilators,

however, compared with that of inhaled bronchodilators

merits further study.

Ketamine

Ketamine is a parenteral dissociative anesthetic that has

been found to be a useful bronchodilator. Most experts think

that ketamine is the anesthetic agent of choice for intubation

of severe asthmatics. Ketamine potentiates catecholamines

and directly induces relaxation of smooth muscle. It also

increases bronchial secretions and can cause emergent reac-

tions. Because of the effect of ketamine on bronchial secre-

tions, atropine (0.01 mg/kg, minimum dose of 0.1 mg) also

should be administered if this agent is used. Benzodiaze-

pines help to minimize emergent reactions, although hallu-

cinations may occur after the patient awakes. The initial

dose of ketamine is 0.1 to 0.2 mg/kg followed by an infusion

of 0.5 mg/kg per hour. In intubated patients or in those being

prepared for intubation, the usual dose of ketamine is a

bolus of 0.5 to 1.5 mg/kg, repeated 20 minutes later, or

infusion of 1 to 5 mg/kg per hour [21].

Heliox

Heliox is a mixture of helium and oxygen (usually 70:30)

that may delay the need for intubation by decreasing the

work of breathing while the other medications are beginning

to take effect [22].

Part 8: Advanced Challenges in Resuscitation280

Bilevel Positive Airway Pressure

Bilevel positive airway pressure intermittently provides

assisted ventilation. Like a combination of positive-pressure

ventilation and PEEP, bilevel airway pressure helps to delay

or abort the need for tracheal intubation. This ventilation

counteracts the effects of auto-PEEP, thereby reducing the

work of breathing. Begin with an inspiratory positive airway

pressure of 8 to 10 cm H2O and an expiratory positive

airway pressure of 3 to 5 cm H2O [23].

Tracheal Intubation With Arti®cial Ventilation

In some patients oxygenation and ventilation can be

achieved only after sedation, general anesthesia, muscle

paralysis, and tracheal intubation. Patients with severe

asthma experience some obstruction of inspiration and

marked obstruction of expiration. This results in auto-

PEEP, which is secondary to air trapping and `breath stack-

ing' (breathed air entering and being unable to escape).

The following critical points relate to tracheal intubation

for life-threatening asthma:

² Provide adequate sedation with ketamine, a benzodiaze-

pine, or a barbiturate.

² Paralyze the patient with succinylcholine or vecuronium.

² Once intubated some patients may need permissive

hypercarbia with elective hypoventilation [24].

² Inhaled volatile anesthetics, although no longer widely

used or available outside the operating room, are power-

ful relaxants of bronchial smooth muscle. Agents such as

halothane, iso¯urane, en¯urane, and ether have been used

to reverse status asthmaticus refractory to all other treat-

ments [25]. Use these agents with extreme caution

because (except for ether) they are also vasodilators

and myocardial depressants. Some anesthetics sensitize

the myocardium to catecholamines, leading to life-threa-

tening arrhythmias.

² Extracorporeal membrane oxygenation has been used as

a lifesaving measure for severe refractory asthma when

all else has failed, but this technique is not generally

available.

² For most experts ketamine is the intravenous anesthetic

of choice for patients with status asthmaticus. In titrated

doses ketamine has a mild bronchodilator effect and does

not cause vasodilatation, circulatory collapse, or myocar-

dial depression.

Steps to Take Immediately After Intubation

Tracheal intubation only provides more external mechan-

ical power to the patient's failing ventilation efforts; it does

not solve the problem. Patients with severe asthma may be

extremely dif®cult to preoxygenate manually before intuba-

tion and even once the tube is in place.

Because breathing efforts may be uncoordinated, the

patient may not have inhaled an adequate amount of b2-

agonist before intubation. Immediately after intubation

inject 2.5 to 5.0 mg of albuterol directly into the tracheal

tube. Con®rm correct placement of the tracheal tube by the

following newly recommended sequence:

² Primary tracheal tube con®rmation. Visualize the tube

past the vocal cords; perform 5-point auscultation; watch

chest rise; condensation in tube. Auscultation can be

misleading because poor ventilation and air movement

may result in inaudible breath sounds in patients with

severe refractory asthma.

² Secondary con®rmation of tube placement. Qualitative

end-tidal CO2 detectors; esophageal detector device;

dynamic pulse oximetry readings; quantitative and

continuous CO2 measurements using capnometers or

capnographs.

Ventilate the patient with 100% oxygen.. The absence of

any signi®cant obstruction to air¯ow immediately after

intubation suggests that the diagnosis of acute asthma may

have been incorrect, and the problem may have been more

in the upper airway (eg, vocal cord dysfunction, tumor, or a

foreign body). The person who performs manual ventilation

after intubation should be instructed beforehand to ventilate

at a rate of only 8 to 10 breaths per minute to avoid auto-

PEEP and its consequences (eg, sudden severe

hypotension). The drop in blood pressure with

hyperventilation may be extremely sudden. Prevention of

this problem is clearly better than treatment of it.

Acute asthma can be confused with exacerbation of

emphysema, especially in the elderly. For different reasons

hyperventilation immediately after intubation can cause dire

consequences in elderly patients with emphysema. (See the

textbook Advanced Cardiovascular Life Support for an in-

depth discussion of this topic.)

Intubated, Critically Ill Asthmatic: Ventilator-Dependent

Permissive Hypercapnia

Adequately sedate and paralyze the patient to allow a

`passive' ventilator-patient interaction. Allow Pco2 to rise

(permissive hypercapnia) to values as high as 80 mm Hg.

The ensuing drop in pH can be controlled with bicarbonate

if needed.

To set the ventilator for permissive hypercapnia:

² Rate: provide mechanical ventilation, 8 to 10 breaths per

minute

² Volume: tidal volume, 5 to 7 mL/kg

² Peak ¯ow: 60 L/min with a decelerating pattern

² Inspired oxygen: Fio2, 1.0 (ie, 100%)

Part 8: Advanced Challenges in Resuscitation 281

If the patient's airway is extremely dif®cult to ventilate,

perform the following procedures in order until ventilation

is adequate:

1. Ensure that the patient is adequately sedated or paralyzed

so that there is passive patient-ventilator interaction.

2. Check the patency of the tube for obstructions caused by

kinking, mucous plugging, or biting. Aspirate the tube as

needed.

3. To ensure that the patient is receiving adequate tidal

volume, increase the time for exhalation, decrease the

time for inhalation, and increase the peak pressure.

4. Reduce the respiratory rate to 6 to 8 breaths per minute to

reduce auto-PEEP to #15 mm Hg.

5. Reduce the tidal volume to 3 to 5 mL/kg to reduce auto-

PEEP to #15 mm Hg.

6. Increase peak ¯ow to .60 L/min (90 to 120 L/min is

commonly used) to further shorten inspiratory time and

increase the ratio of inspired to expired air (I:E) [26].

Troubleshooting: Hypotension or Desaturation Immediately

After Intubation [26]

Ensure that the tracheal tube is in the correct position. The

tube should be inserted to 21 to 23 cm (measured at the

incisors) in most men and to 20 cm in most women.

These values may need to be reduced in a small person.

Incorrect placement of the tube must be addressed imme-

diately. Do not take the time to obtain a chest x-ray,

although an x-ray of the chest after intubation is always

appropriate. The immediate consequences of insertion of

the tube incorrectly in a patient with severe refractory

asthma may be fatal.

If the patient is dif®cult to ventilate, check the patency of

the tube for obstructions caused by kinking, mucous plug-

ging, or biting. Aspirate the tube.

The differential diagnosis of hypotension or desaturation

immediately after intubation, once tube position is

con®rmed, includes tension pneumothorax and massive

auto-PEEP buildup. In patients with severe refractory

asthma the chest often is silent to auscultation because of

poor air¯ow and hyperin¯ation of the chest wall.

Tension Pneumothorax. Evidence of a tension

pneumothorax includes unilateral expansion of the chest

wall, shifting of the trachea, and subcutaneous emphysema.

The lifesaving action is to release air from the pleural space

with needle decompression. Slowly insert a 16-gauge

cannula in the second intercostal space along the

midclavicular line, being careful to avoid direct puncture of

the lung. If air is emitted, insert a chest tube.

Caution! Insertion of a chest tube in a patient with severe

refractory asthma without pneumothorax will have dire

consequences because the visceral pleura of the hyperin-

¯ated lung could be punctured, iatrogenically producing

pneumothorax. The person inserting the tube would not

realize that this has occurred because puncture of the lung

would cause a release of air under pressure through the

needle catheter or thoracostomy tube, just as would occur

with relief of tension pneumothorax. Because of the high

pressures experienced by the contralateral mechanically

ventilated lung and coexisting auto-PEEP, contralateral

pneumothorax would be generated, most likely under

tension.

Massive Auto-PEEP Buildup. The most common cause of

profound hypotension after intubation is a massive buildup

of auto-PEEP. Stop ventilating the patient for a brief period

(,1 minute) and allow the auto-PEEP to dissipate. At the

same time observe the patient's oxygenation.

Hypotension may also be due to the intubation sedatives,

which should respond to volume infusion.

If high auto-PEEP is not present, reconsider alternative

explanations.

² Obtain an ECG: Exclude myocardial ischemia or infarc-

tion as a consequence of acute respiratory failure (ie,

hypoxemia, intubation, and medications) [27,28].

² Request emergency consultation from a pulmonologist.

² Request emergency consultation from an anesthesiolo-

gist.

² Admit the patient to the Critical Care Unit.

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