Sudden Cardiac Arrest and Asthma
Larry Mellick, MD, MS, FAAP, FACEP
Professor of Emergency Medicine
Medical College of Georgia
and
Ryan Johnson, MD
Emergency Medicine Resident
Medical College of Georgia


Pearl: Consider bilateral tube thoracostomies in any asthmatic patient who suddenly deteriorates into cardiopulmonary arrest.

Presentation: A 9 year old female with a history of asthma presented to the ED with dyspnea that began on the afternoon of arrival. Her initial vitals were: temperature 37.8 Celsius, pulse 153, RR 30, SaO2 85% on room air, BP 135/85. Her history was significant for four prior severe asthma exacerbations that required admission to the pediatric intensive care unit. Her home medication included a fluticasone and salmeterol inhaler (250/50), montelukast (5 mg), fluticasone nasal spray and albuterol nebulizations as needed. On exam the patient was in moderate distress, was able to speak in 4-5 word phrases, and demonstrated nasal flaring as well as chest wall retractions. Auscultation of the chest demonstrated wheezing bilaterally. The airway was patent and there was no tracheal deviation, abdominal pain, or external signs of trauma. The patient was presumed to be experiencing an asthma exacerbation and she was treated with 100% oxygen by non-rebreather mask, albuterol and ipratroprium jet nebulizations and 80 mg of oral prednisone. A chest radiograph demonstrated flattened diaphragms and possible atelectasis in the right lower lobe. The patient was given 1 gram of magnesium sulfate intravenously. Because the patient continued to require oxygen and remained tachypneic despite aggressive therapy with repeated jet nebulization treatments, she was admitted to the pediatric intensive care unit (PICU). Shortly after admission to the PICU, the patient suddenly expressed a feeling of impending doom and promptly collapsed. She was intubated orally by rapid sequence induction. Following intubation, ventilation was noted to be difficult and the patient subsequently developed asystole. Bilateral needle decompressions were performed and a return of air was noted. Bilateral chest tubes were inserted and a rush of air from each side was noted. The patient continued in asystole and pericardiocentesis was performed. After more than an hour of advanced cardiac life support (ACLS), further attempts to revive the patient were discontinued. An x-ray demonstrated that air had also disseminated into the peritoneal cavity.

Discussion: The differential diagnoses of fatal or near fatal asthma may include pneumothorax/pneumomediastinum, cardiac arrhythmias, pneumonia, atelectasis, myopathy and sepsis.1 The 1997 advisory statement from the International Liaison Committee on Resuscitation2 and the 2005 European Resuscitation Council Guidelines for Resuscitation 20053 listed the following conditions as having been linked to sudden cardiac arrest in asthmatics.
  • Severe bronchospasm leading to asphyxia
  • Tension pneumothorax, often bilateral
  • Cardiac arrhythmias
  • Use of β-adrenergic agonists
  • Hypotension and bradycardia mediated by vasovagal reflexes
  • Cardiac conduction disease, possibly mediated by an altered immune complex reaction in some patients
  • Auto-PEEP, sometimes, but not always, in patients on mechanical ventilation
The resuscitation literature in near fatal4 and fatal asthma has established that pneumothorax associated with asthma is not an uncommon problem and healthcare providers should consider bilateral chest tubes in asthmatic patients who suddenly arrest. Josephson and Goetting reported in a 1997 abstract that in their small series the rate of pneumothorax in asthmatic cardiac arrests was 75% as compared to 12% in non-asthmatic patients who arrested. 5 They concluded that pneumothorax occurs frequently in asthmatic cardiac arrests, is often unrelated to central line placement, and is difficult to detect clinically. It was their opinion that empiric bilateral chest tube placement should be an essential part of resuscitation efforts during asthmatic cardiac arrests.

Text books teach us the classic findings of tension pneumothorax (TPT) but the experienced clinician and literature shows that the physicians often do not observe the "classic" signs in patients with TPT. 6,7 Further complicating the issue is if bilateral tension pneumothorax are present the "classic" signs may be missing all together.

The use of chest radiograph to diagnose any unstable or severely compromised patient should probably be abandoned because the use of chest radiography to diagnose TPT has been associated with a fourfold increase in mortality. 8,9

Classically we are taught that needle decompression of a possible TPT followed by tube thoracostomy is both diagnostic and therapeutic. There is evidence that needle decompression is often ineffective because of length of cannula, chest wall thickness or insertion technique. 10,11 The lack of a "hiss" or rush of air upon needle decompression should not be used to exclude TPT in all patients with high risk for TPT and reports show that adequate treatment is only achieved by tube thoracostomy. 10-14

Recent literature and expert opinion is now suggesting that bilateral tube thoracostomies be performed in cardiac arrest asthmatic patients. 15,2,6 They have made this recommendation because of the high morbidity of a missed TPT, high incidence of TPT in cardiac arrest asthmatics, unreliable and insensitivity of physical exam radiography, and potential ineffectiveness of needle decompression. The AHA advisory endorses that "Decompression be attempted empirically for refractory patients, even before confirmation of a pneumothorax." 2

References:

  1. Plaza V, Serrano J, Picado C, Sanchis J. High Risk Asthma Research Group. Frequency and clinical characteristics of rapid-onset fatal and near-fatal asthma. Eur Respir J. 2002 May;19(5):846-52
  2. Special Resuscitation Situations. An Advisory Statement From the International Liaison Committee on Resuscitation. Circulation. 1997;95:2196-2210.
  3. European Resuscitation Council Guidelines for Resuscitation 2005 Section 7. Cardiac arrest in special circumstances. Resuscitation (2005) 67S1, S135—S170.
  4. 10.5 Near Fatal asthma. Circulation 2005;112;139-142 http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-139
  5. Josephson E, Goetting M. Asthmatic cardiac arrest: an indication for empiric bilateral tube thoracotomies, Ann Emerg Med 1989;18:457. Abstract
  6. Leigh-Smith S, Harris T. Tension pneumothorax—time for a re-think? Emerg Med J. 2005 Jan;22(1):8-16.
  7. McRoberts R, McKechnie M, Leigh-Smith S. Tension pneumothorax and the "forbidden CXR" Emerg Med J. 2005;22:597–598.
  8. Steier M, Ching N, Roberts EB, Nealon TF Jr. Pneumothorax complicating continuous ventilatory support. J Thorac Cardiovasc Surg 1974;67:17–23.
  9. Kollef MH. Risk factors for the misdiagnosis of pneumothorax in the intensive care unit. Crit Care Med 1991;19:906–910.
  10. Britten S, Palmer SH, Snow TM. Needle thoracocentesis in tension pneumothorax: insufficient cannula length and potential failure. Injury 1996;27(5):321-322.
  11. Britten S, Palmer SH. Chest wall thickness may limit adequate drainage of a tension pneumothorax by needle thoracocentesis. J Accid Emerg Med. 1996;13(6):426-427.
  12. Jenkins C, Sudheer PS. Needle thoracocentesis fails to diagnose a large pneumothorax. Anaesthesia 2000;55:925–926.
  13. Jones R, Hollingsworth J. Tension pneumothoraces not responding to needle thoracocentesis. Emerg Med J. 2002;19:176–177.
  14. Mines D, Abbuhl S. Needle thoracostomy fails to detect a fatal tension pneumothorax Ann Emerg Med. 1993;22:863–866.
  15. Castle N, Tagg A, Owen R. Bilateral tension pneumothorax. Resuscitation. 2005;65(1):103-105.

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