For life-threatening asthma, first gain control with sedation or the paralysis method of your choice — many tout ketamine for this (Ann Emerg Med 1996;27:170) — and then reach for the ET tube. Bag/mask ventilation for severely elevated airway pressure tends to shunt air into the stomach, courting aspiration. Everyone is relieved when a struggling asthmatic is finally intubated, especially if the oxygen saturation is acceptable, but there should be only a modicum of solace at this point. If dynamic hyperinflation of the lungs (auto-PEEP) is severe enough to cause cardiac arrest (usually PEA, bradycardia, or asystole), stop the aggressive ventilation. In fact, disconnect the ventilator tubing altogether, and stop bagging. Compress the chest wall in CPR-like fashion. This, with a period of apnea, may relieve gas trapping if dynamic hyperinflation is the culprit. Although this procedure is supported by limited evidence, it is unlikely to be harmful in an otherwise desperate situation.
Some cardiac arrest situations require special treatments, procedures, or interventions that are beyond those discussed under BLS/ACLS. The new American Heart Association (AHA) guidelines include 15 such circumstances that address a variety of clinical conditions that will result in sudden death. Similar guidelines are in the European Resuscitation Council Guidelines for Resuscitation 2005: Section 7. Cardiac Arrest in Special Circumstances. (Resuscitation 2005;67 [Suppl 1]:S135.)
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Field JM, et al
2010;122(18 Suppl 3):S639
Almost 6,000 asthma-related deaths occur yearly in the United States, often in the prehospital setting, and asthma-related cardiac arrest can be an EMS issue that garners special attention. If you have not yet faced a rapidly deteriorating, if not recently arrested, individual with asthma, you haven't worked enough shifts. Severe asthma is a frightening experience for patients and a prodigious challenge for clinicians. Unfortunately, you just can't save everyone, and the deceased is almost always a young person with “just another asthma attack.” It's very tough to explain that tragedy to relatives.
Asthma usually causes death by asphyxia, secondary to bronchoconstriction, airway inflammation, and mucus plugging but also tension pneumothorax, diffuse atelectasis, pneumonia, and pulmonary edema. The difference between life and death can be one errant yet tenacious mucus plug. Physiologically severe asthma is associated with hypercarbia, acidemia, and hypotension due to decreased venous return. The final common pathway is pulseless electrical activity (PEA) or asystole, so asthma is not primarily a cardiac specific issue.
Oxygen saturation is not always reflective of progressive hypercarbia or hypoventilation, particularly if supplemental oxygen is administered. Beta agonists can produce bronchodilation, vasodilation, and increased intrapulmonary shunting. This is the classic ventilation-perfusion mismatch, so be prepared for the oxygen saturation to fall initially with bronchodilator therapy.
The AHA states that inhaled beta agonists are mainstay therapy, that intermittent versus continuous administration provides equal benefit, and that one can use either a metered dose inhaler with spacer or a nebulizer. Most clinicians don't realize that it requires four to eight full puffs of a personal inhaler to equal one nebulizer treatment. In my experience, severely dyspneic patients seem to do better with the mist than trying to coordinate the metered dose inhaler, and also they have tried the inhaler at home numerous times without relief. Levalbuterol is no better than albuterol. Ipratropium may effectuate modest clinical improvement. Systemic corticosteroids are a must. The AHA does not mention inhaled steroids for acute asthma, but there is support for this intervention. I frequently add 10 mg of decadron to the albuterol nebulizer. Others have had success in acute asthma with frequent doses of Flovent. Magnesium sulfate has some minimal benefit, and is supported for very severe asthma by a Cochrane meta-analysis. (2000; No. 1:CD0011490.) Infusing 2 g IV over 20 minutes is a safe and common practice.
Subcutaneous (or intramuscular) epinephrine or terbutaline are safe, effective, and advantageous if patients cannot tolerate inhalation therapy. I personally reach for epinephrine (1:1000: 0.3 mg/ml) as the patient rolls in with EMS, inject the deltoid as soon as possible, put the vial to the side where I can find it, and aim to repeat this every 20 minutes, regardless of age, heart rate, or blood pressure. (Ann Emerg Med 1988;17:322.) If the thigh is available, it provides the best IM site. Clinical veterans remember when the only treatment available for severe asthma was epinephrine. It worked well, it still works, and it requires no participation by the patient, but most housestaff have never used it and don't even know dose and route specifics. An infusion of epinephrine is mentioned for severe refractory asthma, but there are little data.
An infusion of S-albuterol is used in other countries, but so far this strategy has escaped the perusal of the AHA. Ketamine is weakly endorsed as is BiPAP. Aminophylline is no longer advocated, and heliox has lost its advocates.
Tracheal intubation is axiomatic in the severely affected patient. It's difficult to know exactly when to consider intubation. It always seems too early or too late, so a seasoned clinician's judgment is the best adjunct. The AHA notes that tracheal intubation does not reverse small airway constriction, and intubation should always be followed by bronchodilator therapy while the patient is being ventilated.
The concept of aggressive positive pressure ventilation being harmful or counterproductive for severe asthma is an issue that should be familiar to all EPs. This is clinically manifested when the recently intubated asthmatic deteriorates right in front of you despite a secure airway, good breath sounds, a stellar oximetry, and aggressive bagging with 100% oxygen. Bradycardia, hypotension, and acidosis worsen in a few minutes despite having the airway under control. When that happens, the natural inclination is to ventilate even more vigorously, and that can be your worst intervention.
The end result of excessive ventilation of asthmatics is incomplete air expiration, so-called breath stacking, air trapping, or auto-PEEP. This results in hyper-expanded lungs, high airway pressures, decreased venous return, decreased cardiac output, and occasionally pneumothorax. This is avoided by using a slow respiratory rate, sometimes as low as four to six per minute, and small tidal volumes, such as 6 ml/kg. If you can manipulate the dials on the ventilator, opt for shorter inspiration time and longer expiratory time. It's fine to allow hypercapnia to persist — it's not dangerous, and is well tolerated as long as the patient is oxygenated, and that does not have to be 100%. Few respiratory techs will allow you to keep the ventilator set at six breaths per minute when the PCO2 is 70 mm Hg, but that's exactly what you should do to avoid barotrauma and more hyperaeration. The AHA does not recommend bicarbonate even though the patient is severely acidotic.
If the patient deteriorates despite your ventilation, simply stop ventilating, and disconnect the ventilator tubing. Some clinicians will actually do CPR-like chest compressions only without bagging for 30-60 seconds to expel the trapped air, a sound physiologic principle that seems like a bad idea at first. That's exactly what you should do: pump on the chest, and halt ventilations to decrease intrathoracic pressure and enhance venous return. Higher defibrillation doses are suggested due to increased transthoracic impedance from the overinflated lungs.
When ventilated, the patient should be heavily sedated. I prefer ketamine and benzodiazepines for this, but a variety of standard interventions (propofol being popular) are acceptable, with no single regimen posited by the AHA. Judicious short-term muscular paralysis with sedation is OK also, but the ICU has been decreasing the use of long-term paralytics. The AHA notes four common causes of acute deterioration in any intubated asthmatic: tube displacement, tube obstruction, pneumothorax, and equipment failure.
About 1,000 people die from anaphylaxis each year in the United States, primarily from medications, latex, food, and insects. The AHA has no new insights into anaphylaxis over previous teachings. Actually, there are no randomized controlled trails evaluating various treatments for anaphylaxis, but there are consensus-based therapies. IM epinephrine (0.2-0.5 mg) given in the anterior lateral aspect of the middle third of the thigh produces highest peak blood levels, and it is supported for anaphylaxis. The subcutaneous route is avoided in true hypotensive anaphylaxis. The only drug that apparently saves lives in anaphylaxis is epinephrine.
The judicious use of small aliquots of intravenous epinephrine can be tried for severe anaphylaxis, but adrenaline is a powerful medication when there is any cardiac activity. I would opt for no more than 0.05-0.1 mg per IV dose if hypotension is severe; otherwise IM epinephrine should suffice. Even a small dose of IV epinephrine can cause severe hypertension, headache, chest pain, and myocardial infarction when injected into an intact circulation, and this route should be reserved for the patient in extremis. Alternatively, you could add 1 mg epinephrine (one crash cart vial) to a liter of fluid run wide open, and titrate back to heart rate or monitor findings.
In summary, the AHA says, “It is reasonable to consider the IV route for epinephrine as an alternative to IM administration of epinephrine in anaphylactic shock.” For patients not in cardiac arrest, “IV epinephrine 0.05 to 0.1 mg has been used successfully in anaphylactic shock.” (New Engl J Med 1991;324:1785.) The AHA endorses the continuous infusion of IV epinephrine (5 to 15 mcg/min or 0.005-0.015 mg/min) for true anaphylactic shock for patients not in cardiac arrest. Put 1 mg epinephrine in 1 liter of saline (1 mcg/ml), and for a 70 kg person, run at up to 15 ml/min. Other vasopressors for anaphylaxis have not been well studied. And although antihistamines and steroids are always used, no prospective randomized trials attest to their effectiveness.
Without question, the best hope for fetal survival is maternal survival. During CPR or to prevent impending cardiac arrest, the AHA states that pregnant patients should be placed in a full supine left lateral position to relieve compression of the vena cava by the gravid uterus. Administer 100% oxygen and IV fluids, with the IV site above the diaphragm. As one might suspect, no randomized trials have examined the effect of specialized obstetrical resuscitation versus standard resuscitation. If you can't turn the patient on her left side, manually retract the uterus to the left while the patient is in a supine position. Overall, primary cardiac arrest in a pregnant woman is initially treated the same as in a nonpregnant woman.
The AHA highlights conditions specific to pregnancy. Women who arrest while receiving magnesium sulfate should be treated with empirical IV calcium (give two amps to start). Preeclampsia is best treated by delivery. Pregnant women who have an arrest with pulmonary embolism should be treated by standard methods, including thrombolytics. Amniotic fluid embolism is often fatal, and may require perimortem C-section. Interestingly, emergency C-section can be therapeutic for women in cardiac arrest. One small series recorded spontaneous return of circulation after immediate delivery in 12 to 20 women, with no case reports of worsening maternal status after C-section.
Exactly when to perform a C-section is a gray area, but it is not considered if the pregnancy is under 24- to 26-weeks gestation. Traditionally, a five-minute window post-arrest has been suggested, but if the mother is obviously terminal, it could be done immediately, but requires a lot of help and an aggressive team. It would surely be difficult to do a C-section within five minutes of maternal arrest in most EDs. Infant survival has been documented as long as 30 minutes post-onset of maternal death.
Peripheral venous access can be difficult in the wildly agitated patient, but this is how to gain chemical control of a rapidly deteriorating asthmatic who also may be severely cocaine-toxic, drunk, or psychotic as well as hypoxic. Ketamine (100 mg IV) or similar favorite and appropriate medications can be mainlined into a bulging external jugular vein while the patient is still in the hallway. One assistant lies across the upper chest; another holds the head steady. Usually this overcomes the patient's neck strength. (Don't get bitten.) This tactic can also be used in any peripheral vein. An assistant sits on the lower leg, and the clinician mainlines an ankle vein. If the proper cocktail is chosen, he will stop struggling quickly, the oxygen mask can be reapplied, and a saner intubation commenced. I have also used this technique for succinylcholine, haloperidol, and benzodiazepines. One advantage of ketamine is that 4-5 mg/kg can be given IM,
This is certainly a challenging problem for the clinician, but morbid obesity by itself does not appear to change survival rates for cardiac event. No modifications in BLS/ACLS have been proven effective for the morbidly obese patient. It is always difficult to intubate the obese patient (consider LMA/King airway), and IV access is problematic (consider intraosseous devises).
It is nearly impossible to determine immediately if a cardiac arrest is due to pulmonary embolism (PE). It is largely an educated guess or instinct. A PE can cause PEA, but most cases of PEA are not due to a PE. The AHA states that “in patients with cardiac arrest due to presumed or known PE, it is reasonable to administer fibrinolytics.” If the patient does not have a PE, routine fibrinolytics during CPR have no benefit, and tPA is not recommended routinely for cardiac arrest. If one can presume or diagnose PE, fibrinolytics during CPR may improve the patient's chance of survival, despite the side effects of this intervention. tPA is likely impossible to obtain from the pharmacy in time to be helpful once the code has commenced. Perhaps an emergency echocardiogram can be helpful in determining the presence of a PE, but this is a luxury rarely available in real time. Embolectomy is always mentioned for a PE arrest, but usually that's a fantasy intervention for the ED.
The AHA made no changes in ACLS for severe electrolyte disturbances associated with cardiac arrest, but keep in mind:
Hyperkalemia: Protect the heart with IV calcium; shift potassium into the cells with bicarbonate, insulin/glucose, and nebulized albuterol; remove the potassium with kayexalate and dialysis. The presence of any bradycardic rhythm, not just a wide QRS/peaked T waves, suggests hyperkalemia.
Hypernatremia/hyponatremia: No recommendations.
Hypermagnesemia: IV calcium.
Hypomagnesemia: IV magnesium; can use a 1-2 g bolus if VT/VFR.
Hypercalcemia/hypocalcemia: No recommendations.
Next month: More special situations of cardiac arrest, including toxins, beta blockers, cocaine, and others.
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Dr. Robertsis the chairman of emergency medicine and the director of the division of toxicology at Mercy Catholic Medical Center, and a professor of emergency medicine and toxicology at the Drexel University College of Medicine, both in Philadelphia.
Read all of Dr. Roberts' past columns in the EM-News.comarchive.
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