Emergent transport request
An air medical transport team is called to transfer a 19-year-old male from a small, six-bed freestanding urgent care center in a farming community 50 miles from the regional university-based referral center. The patient has a history of asthma and was hospitalized earlier in the year. He presented to the referral center in extremis, unable to speak in full sentences with intercostal and supraclavicular retractions. Nebulized albuterol and ipratropium bromide (atrovent) failed to improve the patient’s respiratory distress and his trachea was promptly intubated following a period of symptomatic bradycardia and hypoxic cardiac arrest.
Upon arrival of the transport team, the patient is intubated and being mechanically ventilated. He is on volume control ventilation with a tidal volume of 300 ml, a rate of 20 breaths/minute, a minute ventilation of 5 to 6 liters/minute, a fraction of inspired oxygen of 1.0 and a PEEP of 7 cmH2O. His oxygen saturation on the bedside monitor reads 85 percent. A dopamine drip is infusing at 10 mcg/kg/min for a blood pressure of 85/62 (MAP 70 mmHg) and a heart rate of 134 beats/minute. He has been receiving continuous nebulized albuterol through his ventilator circuit. His most recent arterial blood gas shows a pH of 7.05, a PCO2 of 89 mmHg, a PaO2 of 52 mmHg, a NaHCO3 of 24 mEq/L and an arterial oxygen saturation of 84 percent. Is transport safe to commence?
A brief overview of the pathophysiology
Asthma is a restrictive airway disease characterized by three primary alterations in respiratory anatomy: bronchoconstriction, airway inflammation and mucous plugging7. Triggers to acute episodes vary (e.g., allergens, viral and bacterial respiratory infections, stress, etc…), as does the response to treatment. The reasons for the variation include the degree or severity of airway inflammation, the amount of mucous plugging and individual response to management such as inhaled β2 agonists3.
More specific to what would prompt initiation of critical care transfer include the definitions of Status Asthmaticus and Near Fatal Asthma (NFA). Transport is often reserved for acute asthma exacerbations refractory to standard management. Because of this, patients are often more tenuous and require rapid intervention and a keen clinical eye.
Status Asthmaticus2: This is defined as severe, persistent airway obstruction despite initiation of standard acute asthma therapy.
Near Fatal Asthma (NFA)5: This is defined as an acute asthma exacerbation resulting in respiratory failure, hypoxia, hemodynamic and metabolic compromise. If patients survive the inciting episode, they will require ICU admission.
Observational assessments include mental status and work of breathing (diaphoresis, use of accessory muscles, degree of anxiety)4. Tachypnea and tachycardia are common, secondary to sympathetic compensatory responses or inhalational medications initiated prior to transport team arrival. Pulsus Paradoxus (fall in systolic blood pressure during inhalation of 10-25 mmHg) is a common finding but sometimes difficult to assess without invasive monitoring.
Bedside pulmonary function tests are quite useful however, are often not a possibility by the time critical care transport is initiated. Obtaining results of forced expiratory volume (FEV1) or peak expiratory flowrate (PEFR) upon initial consultation in the referring ED are often useful in ascertaining asthma exacerbation severity4. The presence or absence of wheezing in and of itself tells little with respect to the severity of the episode. The presence or absence of wheezing, along with other clinical assessments is quite useful.
Blood gas analysis may help to determine the stage and severity of the patient’s acute exacerbation or response to initiated therapy. While it should not be the initial or primary indicator, a rapid blood gas assessment may be of some use. An early asthma attack may show respiratory alkalosis secondary to tachypnea. As symptoms progress and become more severe, respiratory acidosis and hypoxia will ensue. Late and ominous findings on blood gas will be metabolic acidosis and high lactate levels2.
A short history and rapid physical examination should occur while treatment is initiated. The extent of history taking will be dependent on the patient’s ability to answer questions and the degree of dyspnea. Care should not be delayed to obtain a thorough history and physical examination3. One piece of important assessment information should be determining whether or not the patient has ever been admitted to an ICU or required intubation for their asthma in the past year or have had an NFA episode2. Signs of impending respiratory arrest may include drowsiness or confusion, bradycardia, paradoxical abdominal muscle movement compared to the thorax, absence of wheezing (ie. “silent chest”), poor chestwall excursion and severe hypercarbia and hypoxia as indicated by blood gas analysis2.
Oxygen is utilized to maintain saturations above 90 percent. Intubation and Mechanical ventilation should be avoided if at all possible. High intrathoracic pressures associated with positive pressure ventilation may cause hypotension secondary to decreased veonous return. Vascular crystalloid infusion should be initiated in patients with status asthmaticus in order to correct fluid and electrolyte imbalances3.
Inhaled β2 agonists such as albuterol or levalbuterol (xopenex), in conjunction with an inhaled anticholinergic such as ipratropium bromide (atrovent) has shown to be most effective in reversing bronchospasm2. β2 agonists are short-acting and provide the most rapid initial relief. There is no evidence to show that nebulized medication is more or less efficacious than metered-dose inhalation management7.
Corticosteroid therapy is utilized to address the inflammation component of asthma. The effects however are not apparent for approximately six hours or more2,7. The IV route shows reliable absorption and is typically given as an initial adult dose of methylprednisolone (solumedrol), 125 mg or dexamethasone (decadron), 10 mg7.
Epinephrine or terbutaline injected subcutaneously (SC) also provide a sympathetic response with the goal of bronchodilatation. The dose of epinephrine is 0.01 mg/kg (1 mg/ml or 1:1000 concentration) , divided in to three doses and administered at 20 minute intervals7. The dose of terbutaline is 0.25 mg, administered every 20 minutes for three doses7. There is no evidence that supports the administration of IV or SC adrenergic agents over inhaled β2 agonists7. These agents are often given when an asthma attack is refractory to inhaled adrenergic agents5.
Magnesium Sulfate has proven to be quite effective in reversing bronchospasm, in combination with inhaled agents. Magnesium causes inhibition of calcium channels in bronchial smooth muscle to relieve bronchospasm, independent of inhaled adrenergic agonists or serum magnesium level. Current adult dosing is two grams administered over 20 minutes for status asthmaticus patients 4,7.
Avoiding the ventilator
Numerous anecdotal reports have shown the promise of utilizing ketamine for patients with refractory asthma. Ketamine is a dissociative anesthetic with sedative, analgesic and bronchodilatory properties. When given as an induction agent for intubation, the dosing is 1 to 2 mg/kg IV4.
Numerous recent reports that low dose infusions have effectively diminished bronchospasm, avoiding the need for intubation sound promising in patients of all ages. Bolus dosing followed by low dose infusions of 0.5 to 2 mg/kg/hour have proven effective in children. While randomized control studies are ongoing, clinical practice is showing this therapy to be safe and help keep patients of the ventilator.
Indications for intubation in the patient in status asthmaticus may include4,5:
• Coma or depressed level of consciousness
• Hypoxemia (PaO2 < 60 mmHg)
• Hypercapnia (PaCO2 > 60 mmHg)
• Hemodynamic instability
• Impending respiratory failure or arrest (see above)
When selecting agents to assist in intubation, care should be taken to minimize or avoid exacerbation of bronchospasm. Lidocaine, 1.5 mg/kg IV, given as a premedication, has shown to curb the cough reflex and mitigate reactive bronchospasm8.
Goals of mechanical ventilation should include reversal of hypoxia, prevention of barotrauma or pneumothoraces and minimizing dynamic hyperinflation5. Dynamic lung hyperinflation occurs as a result of increased airway narrowing, and shortened expiratory times which increases the amount of residual air in the thoracic cavity. Intrinsic positive end expiratory pressure (PEEP) increases and systemic venous return decreases, reducing cardiac output5.. Permissive hypercapnia may be employed until airflow is improved in order to reduce alveolar distention1.
Initial ventilator settings may include1,5:
- Volume OR Pressure control (watch for variations in pressures or volumes depending on the type of ventilation employed)
- 8-12 breaths / minute to allow for optimal exhalation and flow rates (goal I:E ratio should be 1:4)
- Tidal Volume 5-10 ml /kg for maximum plateau pressure of 35 cmH2O
- Equivalent peak inspiratory pressure (PIP) to minimize the effects of overpressure and alveolar overdistention
- Set PEEP of 0 (monitor for intrinsic PEEP)
- FiO2 to maintain oxygen saturations > 90%
Sedative agents to facilitate mechanical ventilation may include ketamine or diprivan (propofol) infusions for their rapid onset and bronchodilatory properties.
Noninvasive positive pressure ventilation (NPPV) has also shown to be of some use in relieving dyspnea associated with respiratory muscle fatigue and improving ventilation to the terminal airways. If this therapy is employed, it is imperative that the patient has adequate negative inspiratory force. Application of this therapy early on may improve the chances that the patient will avoid invasive ventilation. Bilevel positive airway pressure (BiPAP) may prove to be more comfortable for patients than traditional continuous positive airway pressure (CPAP) and may serve as a conduit for inhaled adrenergic agents5.
Our 19-year-old male…
Transport team interventions included ventilator manipulation to maximize exhalation time and minimize intrinsic aPEEP. Tidal volume was increased and plateau pressures were monitored and remained less than 30 cmH2O. The patient received continuous inhaled adrenergic agents and diprivan for sedation. The dopamine infusion was decreased incrementally and eventually discontinued just prior to landing at the tertiary care center.
In the ICU the patient received an inhalational anesthetic desflurane in order to provide added relaxation, dilatation of the airway smooth musculature and reversal of bronchospasm6. This therapy proved to be extremely effective. The patient was extubated within 24 hours and was discharged home 72 hours later. He is receiving follow up care with the asthma clinic at the referral center.
Status asthmaticus and Near fatal Asthma (NFA) can pose a significant challenge to critical care transport providers. Management of hypoxemia and reversal of deadly bronchospasm should be priorities. Patients can become quite tenuous in the transport environment so close monitoring and a well thought out treatment plan is essential.
1. Anderson, ML, & Younger, JG. (2010). Mechanical ventilation and noninvasive ventilatory support. Marx et al. (Ed.), Rosen’s Emergency Medicine (7th ed) (pp. 23-27). Philadelphia, PA: Mosby Elsevier.
2. Katsaounou, PA & Vassilakopoulos, TT. (2009). Severe Asthma Exacerbation. A Gabrielli et al (ed.), Civetta, Taylor and Kirby’s Critical Care (4th Ed). (pp 2110-2133). Philadelphia, PA: Lippincott, Williams and Wilkins.
3. Lazarus, SC. (2010). Emergency treatment of asthma. New England Journal of Medicine, 363(8), 755-763.
4. Nowak RM & Tokarski GF (2010). Asthma. Marx et al. (Ed.), Rosen’s Emergency Medicine (7th ed) (pp. 888-903). Philadelphia, PA: Mosby Elsevier.
5. Restrepo, RD, & Peters, JG. (2008). Near-fatal asthma: recognition and management. Current Opinion in Pulmonary Medicine, 14, 13-23.
6. Tobias, JD. (2009). Inhalational anesthesia: basic pharmacology, end organ effects, and applications in the treatment of status asthmaticus. Journal of Intensive Care Medicine, 24(6), 361-371.
7. Vanden Hoek TL et al. (2010). Part 12: Cardiac Arrest in Special Situations. 2010 Anerican Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Supplement to Circulation 122(18): Supplement 3. November, 2, 2010. (pp. S829-S832).
8. Walls RM(2010). Airway. Marx et al. (Ed.), Rosen’s Emergency Medicine (7th ed) (p. 16). Philadelphia, PA: Mosby Elsevier