Notes from the Chair
Michael Hewitt, RRT-NPS, FAARC, FCCM
Greetings to all from sunny Florida. I completed my move from Maryland right after the AARC Congress and have assumed my new position at the St. Joseph’s Hospitals. This is a great opportunity, and I’m raring to go.
We had another very successful International Congress this past December. About the only downside to this great event was the very atypical weather in San Antonio. However, that did not dampen any of the enthusiasm, nor did it affect the quality of the Congress. Mike Gentile and his committee once again produced an outstanding program that reached across all areas related to respiratory care and all age groups. Our section meeting enjoyed a good attendance as well, and we were pleased to recognize our 2009 Specialty Practitioner of the Year, Matthew Davis, RRT.
As the chair of our section, I also have the privilege of being on the Board of Directors. Under the leadership of President Tim Myers, the board had a busy and productive two-day session just prior to the annual conference. There are continuing issues and concerns being addressed, and 2010 promises to be busy and productive for the board.
One item of particular interest to me is what the future holds for our patients and therapists in the home care setting. I firmly believe that there is a huge potential and opportunity for respiratory therapists in this arena. I am currently working with Bob McCoy, chair of the Home Care Section, and Dr. Kent Christopher, of the AARC’s Board of Medical Advisors, to develop a structured process that will involve RTs in both the transition of the patient to home and continued monitoring while at home.
There are significant issues around this concept, many of which are related to reimbursement. However, I truly believe that with continuing declines in reimbursements, along with stricter readmission/reimbursement criteria being developed by the federal government, we must focus a robust effort in this area. I personally will be meeting soon with the administrative group over our system’s home care division to begin the process of building such a program and to pilot it within our system. I have great enthusiasm for this project and am blessed with some therapists who have specific interest in this area. I even coined a new name for these therapists: “transitionalists.” I may ultimately be proven wrong in this whole idea, but I don’t think that is going to be the case.
Finally, now that the Congress is behind us, we will very soon be launching the Adult Acute Care Section Swap Shop. Joy Hargett and the group we have put together within the section are hard at work with Sherry Milligan in the AARC office, and the launch is getting closer.
I hope you all had a happy, healthy, and safe holiday season. We have a lot to be thankful for. Please keep in mind how privileged we are to be entrusted with the care of the citizens of our community, and that with that privilege comes an awesome responsibility. Let’s embrace that responsibility and do even greater things for our patients and their families in 2010.
I look forward to hearing from you and seeing many of you as I travel about the country. Remember to recruit new members for both the AARC and the section.
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Chemical/Biological Agents
by Joe Hylton, RRT-NPS, CPFT, NCEMT-B
Chemical agents have traditionally been defined as substances intended for use in military operations to kill, seriously injure, or incapacitate humans through their toxicological effects. Chemical agents have been used in warfare for thousands of years, moving to the forefront in World War I. Chemical agents gained attention in the Iran–Iraq war in the 1980s, and in 1994–1995 in Japan, with a terrorist group releasing Sarin.
Chemical warfare agents are classified by their physiological action or military use. Each class of agent causes different pathophysiologic signs and symptoms, thus requiring different care paths. The classes, based on physiologic action, are nerve agents, vesicants, cyanides, pulmonary agents, and riot control agents. The identity of the agent is usually unknown in the initial exposure and treatment, so recognition of signs and symptoms of chemical warfare agents is vital to proper treatment. PPE must be administered to caregivers, and decontamination of the casualties must take place, preferably prior to arrival at the hospital.
Initial management
Staff protection from contamination must be considered, and is vitally important. Protective gear, based on the threat level of the agent, must be provided and trained with to keep caregivers protected from the agent. An established, rehearsed decontamination, and adequate equipment to support the decontamination process, must be in place. This is the most important piece of treatment, and one cannot assume that it has occurred. The Sarin Gas attack in 1995 in Tokyo is a glaring example, as many casualties arrived at health care facilities without being decontaminated.
Decontamination begins with fully exposing the patient; all clothing must be removed, bagged, and labeled. Ideally, decontamination should occur at the scene, prior to transport. Again, the receiving facility should not assume that patients have been decontaminated, and should have the capability to complete this process prior to the patients entering the hospital ED. Disaster tents should be set up to limit weather exposure, and heaters/blankets should be provided to prevent hypothermia. There should be a minimum of two lanes for decontamination; one for patients who can walk, and one for non-ambulatory patients. Commercial agents are available for decontamination, but up to 95% of chemical agents can be effectively removed with scrubbing and water.
Nerve agents
Nerve agents were developed for military use in the 1930s in Germany. These nerve agents include Sarin (SA), Tabun (GA), Soman (GD), Cyclosarin, and Methylphosphonothioic Acid. Chemically, they are related to organophosphate insecticides. The toxicity of these agents lies in their ability to inhibit acetylcholinerase, which results in an accumulation of acetylcholine at the cholinergic synapses. This causes overstimulation of nervous impulses and a resulting cholinergic crisis. The inhibition is initially reversible, but the bond may undergo a secondary reaction known as aging, which produces an irreversibly inactivated enzyme.
Cholionergic receptors are located in the central nervous system, eyes, respiratory tract, bladder, cardiac muscle, sweat glands, and blood vessels. They are divided into two classes, muscarinic and nicotinic. Both receptor sites can be overstimulated by acetylcholine. Muscarinic stimulation results in complications of the eye, respiratory tract, gastrointestinal tract, and cardiovascular system. Nicotinic stimulation results in increased fatigability and generalized weakness, as well as scattered fasciculations, twitching, and cramps.
The presence of signs and symptoms varies with the route of exposure. Inhalation exposure can produce symptoms within seconds, while dermal exposure can take up to 30 minutes and can be delayed for up to 18 hours. Miosis, eye redness, headache, eye twitching, watery nasal discharge, chest tightness, wheezing, tachycardia or bradycardia, anxiety, jitteriness, restlessness, tremors, drowsiness, memory impairment, coma, loss of reflexes, and Cheyne-Stokes respirations may present. Death is usually resulting from respiratory failure, caused by paralysis of the respiratory muscles, loss of airway control, and profound bronchorrhea. The acronym SLUDGE can be used to remember the events: Salivation, Lacrimation, Urination, Defecation, Gastric distress, and Emesis.
Management of nerve agent exposure is vital to survival. Decontamination prevents further exposure of the agent to the patient and the caregivers—decontamination must be dermal, removing clothing and washing the skin, to remove the agent. Endotracheal intubation may be required as opposed to supraglottic devices, due to the potentially high airway pressures required to ventilate the patient. Atropine and Pralidoxime Chloride (2-PAM) are the primary antidotes for exposure, with Diazepam used as an anticonvulsant for seizures.
The recommended dose for Atropine is 2 mg IV, repeated every 5-10 minutes until ventilation is easy and bronchial secretions have decreased. Doses up to 40 mg and higher have been seen in organophosphate poisoning. Atropine does not regenerate acetylcholine. Pralidoxime Chloride (2-PAM) reverses the chemical binding of the nerve agent to acetylcholine, regenerating acetylcholinesterase and allowing the enzyme to metabolize acetylcholine. 2-PAM dosing ranges from 600-1800 mg IV over 20-30 minutes, with a maximum dose of 2 grams/hour. Diazepam is usually administered IV, with a dosage range of 5–10 mg every 10–20 minutes, not to exceed 30 mg in an 8 hour period.
Vesicants
The most commonly known vesicant is Sulfur mustard (Mustard gas, HD). Other agents are Lewisite (L), Nitrogen mustard (HN), and Phosgene oxime (CX). These compounds act as alkylating agents, affecting the biological processes such as cell division and DNA synthesis.
A diagnosis of exposure to vesicants is done through presentation. Vesicants blister the skin and destroy the epidermal layer. They may also act on the eyes, mucous membranes, lungs, skin, and blood-forming organs. The organs most affected are the eyes, mucous membranes, the respiratory tract, and occasionally, the GI system. Severity and duration of symptoms depends on the agent concentration and time of exposure. The hallmark sign of dermal exposure to mustard is a prolonged asymptomatic period, before symptoms begin to occur. It may as little as an hour, to over 12 hours, with the latent period depending on the concentration of the agent, the mode of exposure, and the temperature of the patient. High temperatures and wet skin are associated with severe lesions and shorter latent periods. Inflammation will occur, followed by lesions, then desquamation. Photophobia, lacrimation, irritation, bleophasm, and hemorrhagic conjunctivitis may appear with an ocular exposure. Inhalation will produce bronchial lesions. Sinus pain, nasal irritation, sore throat, hacking cough, hoarseness/loss of voice, shortness of breath, productive cough, purulent bronchitis, and patchy pneumonia may present. Suffocation can present, in response to pseudomembrane development, obstructing bronchi or the trachea.
Treatment of exposure is supportive, with the majority of patients surviving. Early decontamination of the patients and PPE for the caregivers is vital. Maintaining an aseptic environment for the patients is very important, as desquamation has heightened their chances of infection. Topical antibiotics, ophthalmic antibiotics and lubricants, bronchodilators, and IV antibiotics may be required. If airway pseudomembranes develop, bougienage may be required.
Cyanides
Cyanides are commonly known as Hydrogen Cyanide (AC), Cyanogen Chloride (CK), and cyanide salts (sodium cyanide and potassium cyanide). They are often referred to as blood agents, because they are uptaken by the blood or lymphatics and systemically distributed to the tissues and organs. The cyanides interfere with aerobic respiration, stopping the production of ATP and leading to a loss of energy required for metabolism. A metabolic breakdown occurs, despite a normal oxygen supply.
Like other agents, the symptoms depend on the concentration of the agent and the time of exposure. The smell of cyanide has been associated with bitter almonds. The clinical syndrome mimics hypoxia, with the caveat being absence of cyanosis. A high arterial and venous PO2 will be present, but the tissues will be unable to utilize the available oxygen. Symptoms are similar to a cold in the nose and throat at low concentrations, up to gasping for breath, immediate loss of consciousness, convulsions, and respiratory failure leading to death in 1–15 minutes at high concentrations.
Treatment involves removing the patient from the exposure, providing oxygen and assisted ventilations if necessary. Amyl Nitrate via inhalation with one ampule every 3–5 minutes can be effective. Intravenous sodium nitrite (sequesters cyanide on methemoglobin), 300 mg over 5–10 minutes, and sodium thiosulfate (combines with free cyanide to form thiocyanate), 12.5 mg over 10 minutes, can be effective. Hydroxocobalamin (binds directly to cyanide) can be administered intravenously, at 5–10 mg.
Pulmonary agents
Chlorine (CL), Phosgene (CG), Diphosgene (DP), and Chloropicrin (PS) are the most notable pulmonary agents. These agents can cause noncardiogenic pulmonary edema and irritation to the eyes and respiratory tract, and can predispose the patient to a secondary pneumonia. Phosgene is the most commonly used, dating back to World War I. Phosgene is a colorless gas that causes pulmonary edema when inhaled. It is not easily absorbed through the skin.
The hallmark sign of Phosgene poisoning is massive pulmonary edema. Shortness of breath, chest tightness, laryngospasm, wheezing mucosal/dermal irritation, coughing, a burning sensation on the eyes and throat, and blurred vision may be seen. Dyspnea, coughing, and tachypnea usually precede pulmonary edema. If the patient survives the exposure, symptoms usually begin to resolve within 48 hours, provided there is no secondary infection.
There is no specific treatment for exposure. Removing the patient from exposure to the agent is vital, with care being supportive. Bronchodilators/drying agents (Ipratropium), corticosterioids, oxygen, and airway management/assisting with ventilations may be required.
Riot control agents
Chloroacetophenone (Mace, CN) and Ortho-chlorobenzylidenmalononitrile (CS) are riot control agents that are utilized to temporarily incapacitate individuals, and not to kill or injure.
They act on the eyes and mucous membranes, causing intense pain and lacrimation. High concentrations may cause nausea and vomiting. The onset of these agents is felt almost immediately, and may last up to 15 minutes. Diagnosis is made by the presence of their odors, and the presence of ocular and respiratory effects. The agents may exacerbate pre-existing pulmonary disease.
Care of individuals with exposure to riot control agents is supportive. Removal of clothing and eye irrigation is usually required. Oxygen and bronchodilators may be used if symptoms are present.
Conclusion
Appropriately designed disaster plans that are constantly reviewed and rehearsed, and adequate supplies in the event of an incident, are mandatory for successful event management and patient/caregiver survival. Management of patients experiencing exposure to chemical agents requires quick action from pre-hospital agencies and hospitals. The agents must be quickly identified, and appropriate decontamination must occur, preferable at the scene of the event, prior to patient entry into ambulances.
Hospitals should possess the ability to decontaminate patients prior to their entry into the ED, to protect other patients and caregivers. Appropriate personal protection gear must be available to caregivers, and they must be familiar with use of the gear before an event occurs. Proper identification of the agent used, through pre-hospital methods and by patient symptoms, is vital to guiding the patient through the appropriate treatment pathway, to provide an optimal situation for patient and caregiver survival.
References
- Fundamental Disaster Management. Society of Critical Care Medicine, Third Edition, 2009
- Hogan DE, Burstein JL. Disaster Medicine. Lippincott, Williams & Williams 2007.
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Review and Management of Carbon Monoxide Poisoning Part 4: Management
by Russell W. McCord, BA, BSE, RRT-NPS, RPFT, Director of Clinical Education-Respiratory Care Program, Victor Valley College, Victorville, CA
Thank you for following this series on carbon monoxide poisoning. Previously, we have reviewed the properties of CO, its sources, and who is at risk. We examined CO’s increased affinity for hemoglobin and the mechanisms for toxicity. We have also identified the acute and chronic signs and symptoms of CO poisoning, as well as the methods for diagnosis. Now let us look at the management of CO poisoning.
In a 1998 article in The New England Journal of Medicine, Ernst and Zibrak pointed out that the CO-intoxicated patient must first be removed from the source by emergency personnel wearing breathing apparatus. Treatment for CO poisoning involves giving the patient as much oxygen as possible with the purpose of reducing the half life of carboxyhemoglobin (HbCO). It is our desire to administer 100% oxygen so that it may compete with the binding sites of hemoglobin and improve tissue oxygenation. However, it has been recently reported in animal studies that a small fraction of free CO dissolved in plasma also plays an important role in the pathophysiologic consequences. Aggressive respiratory and supportive care should be considered, including protecting the airway with airway management (especially with patients rescued from a fire), blood pressure support, and cardiovascular stabilization.
Previously, we gained understanding of hemoglobin’s tense and relaxed states from Biochemist Brendan Gongol. Gongol also gives a good explanation of how CO is released from hemoglobin. The tense and relaxed states are like an on-off switch for the iron (Fe) center of the hemoglobin molecule. During the relaxed state, the attached CO is exposed. Because the hemoglobin molecule is in a constant state of vibration, it is likely that CO will be kicked off the hemoglobin molecule during its release phase. Studies show that during one atmosphere (atm) of normobaric oxygen (NBO2), 100% oxygen via a non-rebreather mask reaches a pressure in plasma of 637 mmHg. Hyperbaric oxygen (HBO2) provides 100% oxygen under three atms of pressure and reaches a pressure in plasma of 2,193 mmHg. When hemoglobin is in the relaxed state, CO vibrates off the hemoglobin molecule. With NBO2, there is a greater possibility of oxygen attaching to the hemoglobin due to the competitiveness of the larger number of O2 molecules in the plasma, resulting in the eventual displacement of CO. When 100% O2 is delivered under three atms of pressure via HBO2, there is a much greater possibility of oxygen attaching to hemoglobin due to the increased competitiveness. Thus, CO half life is reduced more rapidly with HBO2 than NBO2.
Elimination of CO is related to minute ventilation and duration of exposure, and by improving the O2 content of the blood by maximizing the fraction dissolved in plasma. High-flow oxygen therapy should be administered immediately to treat the hypoxia and accelerate the elimination of CO from the patient. Patients should receive 6–12 hours of 100% oxygen delivered by a high flow oxygen delivery device.
Presently, the oxygen device of choice is a tight fitting non-rebreather mask with all it’s one way valves in place. However, current respiratory care textbooks no longer consider the non-rebreathing mask a high flow device. Furthermore, manufacturers have removed one of the one way gaskets on the mask to improve patient safety. Because of this, there is a controversy over the effectiveness of the non-rebreather mask. Is the non-rebreather mask really delivering 100% oxygen? If not, is there another device that would be more efficient? With the non-rebreather mask, oxygen flow is often delivered at 15-20 LPM with special attention paid to the patient’s minute ventilation. However, there is a new device available called the OxyMask which can run up to 40 LPM of oxygen and advertises an obtainable FiO2 of 0.90.
Consider the VISION—which many hospitals own. With a full-face mask and the ability to dial in CPAP, FiO2 of 1.0, and offering flow compensation, wouldn’t the Vision be a more effective device in reducing the half life of CO? With a properly fitting full face mask and the dialed in FiO2 of 1.0, intuitively it sounds like a better choice than a non-rebreather mask. Could the use of CPAP reduce the airway resistance for a patient who inhaled hot gas during a fire, as well as improve FRC, provide adequate lung volume, and improve oxygenation? Future studies may hold the answer to these questions and offer new possibilities for effectively managing the patient exposed to CO.
Infants and children follow the same protocols as adults. It has been reported that pregnant women may require longer NBO2 treatment than non-pregnant patients. Once treatment begins, O2 therapy and observation must be continued long enough to prevent the delayed pathological condition as carboxymyoglobin unloads. Another controversy is whether 100% oxygen should be administered at normal atmospheric pressure or under increased atmospheric pressure. Recent data demonstrate the benefits of HBO2; however it is not risk-free, and it is not readily available in some communities.
Reports of HbCO half life vary. Weaver, Howe, Hopkins, et al., report in a 2000 issue of Chest that the half life of CO when breathing 100% oxygen at ambient pressure is about 74 minutes, with a range of 26–148 minutes. Because individual variations are determined by the length of CO exposure, prolonged half life may exist. The following table comes from Robert L. Wilkins in chapter 11 of the Ninth Edition of Egan’s Fundamentals of Respiratory Care. The half life of HbCO at different oxygen exposures:
HbCO Half life (minutes) |
Inhaled FiO2 |
PaO2 (mmHg) |
280–320 |
0.21 at 1 atm |
100 |
80–90 |
1.0 at 1 atm |
673 |
20–30 |
1.0 at 3 atm |
2193 |
HBO2 was first introduced in 1890 and first used in the 1960s. During that time, CO toxicity was thought to result entirely from the anemia created by CO-Hgb. It was believed that the benefit of HBO2 came from the accelerated dissociation of CO from hemoglobin. Since then, the mechanisms of CO poisoning and of HBO2 have evolved. Recent animal studies show that HBO2 not only reduces CO binding from hemoglobin, but reduces CO binding from other heme-containing proteins. Other animal studies have shown HBO2 to have the following effects:
- Alter neutrophil adhesion to endothelium
- Decrease free radical-mediated oxidative damage
- Reduce neurologic deficits
- Reduce mortality
Not all animal studies have been positive:
- Does not prevent neuronal injury
- May increase oxidative damage resulting from an increase in oxygen free radicals
Besides the rapid reduction of CO-Hgb levels, other rationales for using HBO2 therapy include the reduction of intracranial pressure and cerebral edema due to the induced cerebral vasoconstriction as well as the rapid dissociation of CO from respiratory cytochromes. Weaver, et al., conclude in their 2002 abstract, “Three hyperbaric-oxygen treatments within a 24-hour period appear to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning.”
Hopkins, et al., conclude in their 2007 article, “Hyperbaric oxygen therapy reduces cognitive sequelae following CO poisoning in the absence of the epsilon4 allele. Since apolipoprotein genotype is unknown at the time of poisoning, we recommend patients with acute CO poisoning receive HBO2”.
Stoller states in a 2007 article, “Hyperbaric oxygen benefits the brain more than normobaric oxygen by, e.g. improving energy metabolism, preventing lipid peroxidation and decreasing neutrophil adherence.”
Koa and Nanagas detail many studies in their 2004 article and agree that more research is needed to resolve the controversy regarding HBO2 and CO poisoning: “Some believe that withholding HBO2 from CO-poisoned patient[s] in future trials would be unethical because of their firm belief in the efficacy of this treatment. Others believe that further trials would be unethical because the paucity of data regarding the effectiveness of HBO2 therapy does not justify the risk and expense of transferring patients to HBO2 treatment facilities. Others have expressed concern that HBO2 supporters seem to be in facilities that offer HBO2.”
There is no widespread agreement on which CO-poisoned patients should be selected for HBO2. Moreover, there is no reliable method available for identifying patients who are at high risk for neurologic sequelae. Based on the current evidence, HBO2 should be recommended for CO poisoning if the patient has significantly high CO-Hgb levels and a history of loss of consciousness, neurological symptoms, cardiovascular dysfunction, metabolic acidosis, and/or abnormalities on neuropsychometric testing. HBO2 is recommended if there is evidence of an elevated maternal CO-Hgb level (>15–20%) and/or evidence of fetal distress. The safety of HBO2 in pregnancy has been questioned, but many agree that HBO2 will be a benefit to the mother and fetus, and because of the difficulty of assessing intrauterine hypoxia. HBO2 should be considered when severe cases of CO toxicity present high COHb levels with signs and symptoms of palpitations, dysrhythmias, hypotension, myocardial ischemia, cardiac arrest, respiratory arrest, and non-cardiogenic pulmonary edema, and for persistent symptoms despite NBO2. Many practitioners use a CO-Hgb level >25% as a criterion for HBO2.
Outcome studies of HBO2 have not, at this time, identified other circumstances in which this therapy is indicated. HBO2 is particularly disputed for patients who are mildly to moderately compromised with cerebral dysfunction.
In a 2004 issue of Emergency Medicine Clinics of North America, Kao and Nanagas reported the following indications for HBO2 therapy in CO poisoning:
Currently Accepted Indications:
- Neurologic findings
a. Altered mental status
b. Coma
c. Focal neurologic deficits
d. Seizures
- Pregnancy with CO-Hgb levels >15–20%
- History of loss of consciousness
Consider for:
- Cardiovascular compromise (ischemia, infarction, dysrhythmia)
- Severe metabolic acidosis
- Extremes of age
- Elevated CO-Hgb level (>25–40%)
- Abnormal neuropsychometric testing results
- Persistent symptoms despite normobaric oxygen
HBO2 consists of the delivery of 100% oxygen within a pressurized chamber, resulting in a manifold increase in the dissolved oxygen in the body (partial pressure of oxygen up to 2,000 mmHg). One hundred percent oxygen at normobaric pressure provides 2.09 vol% or about one third the body’s requirements. At 2.5 atms, 100% oxygen provides 5.62 vol%. In the1959 article, “Life Without Blood,” Boerema, Merne, Brummelkamp, Bouma, Mench, and Kameramans noted that porcine studies illustrated that HBO2 at 3.0 atms provided enough dissolved oxygen to supply the body’s needs in the near-absence of hemoglobin.
HBO2 is not risk-free. Common complaints from patients include painful barotrauma affecting the ears and sinuses, and claustrophobia. Less common risks include:
- Oxygen toxicity
- Seizures
- Pulmonary edema and hemorrhage
- Decompression sickness including pneumothorax and nitrogen emboli
- Fire hazard
The only absolute contraindication to HBO2 is an untreated pneumothorax. Other contraindications include wheezing or air trapping, which can lead to pneumothorax, high fever, and a risk of seizures. Relative contraindications include:
- Claustrophobia
- Otosclerosis or other scarring of the middle ear
- Bowel obstruction
- Significant emphysema with bullae formation
- Care requirements that go beyond what is possible in the HBO2 environment.
Sheridan and Ritz, publishing in Respiratory Care Principle & Practice in 2002, describe how adequate preparation must be made for patients who are mechanically ventilated to prevent complications before closing the HBO2 chamber door. The endotracheal tube cuff must be deflated and refilled with the appropriate amount of saline in order to prevent collapse of the cuff during the compression phase of therapy. Stabilization of the OETT is very important since a patient may awaken in the chamber and attempt to self-extubate.
With this in mind, it is a good idea for the patient to be well restrained, regardless of his mental status, before sealing the chamber door. Ventilator patients also need to be assessed for bronchospasm and aggressively treated with bronchodilators before beginning HBO2. Special care should be given to the removal of both oral secretions and those from the lower respiratory tract—this cannot be performed once HBO2 begins. Tiny prophylactic incisions in the ear drums (myringotomies) should be considered to prevent tympanic membrane rupture in unconscious patients.
Unstable patients are poor candidates for HBO2 because of the compromised access in a monoplace chamber. In addition, if a patient requires emergency defibrillation while undergoing HBO2, it will take several minutes to decompress the patient safely before interventions can be administered. Patients who are at risk for emergent cardiovascular decompensation should be identified before they enter the HBO2 chamber. It is difficult to define a standard of care regarding HBO2 for patients with CO-poisoning. A risk-benefit analysis should be considered for each patient.
Modified versions of pressure-limited, time-cycled ventilators are used in a monoplace HBO2 chamber. A base rate is delivered, but all spontaneous breathing efforts by the patient are unassisted. It may be best to adequately sedate the patient to avoid spontaneous breathing during HBO2. A patient who wakes suddenly and begins vigorously breathing and/or coughs can become at risk for aspiration of oral secretions, which can lead to increased airway resistance as evidenced by increased airway pressures and a reduction of tidal volume. These clinical signs can also be seen with a kinked OETT, pneumothorax, bronchospasm, or mainstem intubation. Because the RT is isolated from the patient, assessment of the patient can be challenging.
HBO2 regimes vary. Typically, HBO2 is delivered with 2 or 3 atms for 90 minutes with three 10 minute room air breaks to reduce the incidence of oxygen toxicity seizures. It has been reported that normobaric oxygen should not be used between multiple hyperbaric oxygen treatments.
The jury is still out on the use of NBO2 versus HBO2. However, a knowledgeable RT who is skilled with patient assessment techniques and is able to weigh the risk versus gain can be a powerful resource to the health care team and help provide a positive outcome for the patient.
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