Until recently, options for the treatment of severe acute respiratory failure were limited. If a patient progressed to the point were he was unable to sustain adequate oxygenation and ventilation on his own, then endotracheal intubation and positive pressure ventilation with a mechanical ventilator became necessary. In the past several years, more aggressive medical therapy with agents such as bronchodilators or nitrates (depending upon the underlying etiology), has resulted in less frequent need for intubation. However, the increasing use of noninvasive ventilatory support (NIVS) has further decreased the need for endotracheal intubation in this patient population. Indeed, the use of NIVS in the Emergency Department is probably one of the most significant advances in the care of patients with acute respiratory failure in recent years. The primary goals of this discussion will be to familiarize physicians with the many advantages of NIVS, to encourage its routine use, and to compare and contrast Continuous Positive Airway Pressure (CPAP) with Bi-level Positive Airway Pressure (BiPAP).
There are many possible etiologies for acute respiratory failure and the diagnosis is often unclear or uncertain during the critical first few minutes after ED presentation. Since it is often necessary to initiate treatment before a clear diagnosis can be established, taking a pathophysiologic approach towards the patient can be useful. To that end, the "respiratory equation of motion" can provide a useful conceptual framework in determining why the patient is unable to sustain adequate minute ventilation.
Pmuscle + Papplied = E(Vt) + R(V) + threshold load + Inertia
Pmuscle is the pressure supplied by the Inspiratory respiratory muscles; Papplied is the inspiratory pressure provided by mechanical means; E is the elastance of the system; R is the respiratory system resistance; Threshold load is the amount of PEEPi or intrinsic PEEP the patient must overcome before inspiratory flow can begin; Vt and V are the tidal volume and the flow rate respectively; Inertia is a property of all mass and has minimal contributions and thus can be ignored clinically.
More simply put, acute respiratory failure results when there is an imbalance between the respiratory muscle power available (supply) versus the muscle power needed (demand). This usually occurs when the respiratory loads are increased to the point where the respiratory muscles begin to fatigue and fail. As examples, acute bronchospasm due to asthma or COPD places an increased resistive load on the respiratory system, acute pulmonary edema decreases lung compliance and thus places an increased elastance load on the system, and in COPD intrinsic PEEP increases the threshold load. The object of medical therapy is to decrease or reverse these acute respiratory loads thereby decreasing demand on fatiguing respiratory muscles. If this is not successful, then ventilation needs to be aided by mechanical means. Recruitment of accessory muscles of respiration and abdominal paradox are clinical signs that the respiratory muscles do not have enough power on their own to meet demand. Any patient with these signs will need to have the loads reduced or eventually, ventilation aided by mechanical means.
Certainly, early aggressive medical therapy is a cornerstone in preventing intubation. If moderately severe acute respiratory failure is not treated very aggressively from the outset a rapid downward spiral with a crash situation can result. For example, in flash pulmonary edema, hypoxia occurs due to V/Q mismatch and shunting, the work of breathing is increased due to bronchospasm and decreased compliance. The hypoxia leads to a rapid shallow respiratory rate, which further increases the work of breathing. The hypoxia and metabolic acidosis further impair respiratory muscle function and also impair cardiac function. A vicious circle ensues whereby respiratory failure aggravates myocardial function and metabolic status aggravates respiratory status. Accessory muscle use is increased to compensate for the increased resistance and decreased compliance. Intrathoracic pressure swings become more pronounced again increasing the work of breathing. Eventually diaphragmatic and other respiratory muscles fatigue, there is further worsening of resistance and compliance, air trapping leads to increased intrinsic PEEP, and there is accumulation of secretions. Severe hypoxia, hypercarbia, metabolic acidosis, and decreasing cardiac output eventually lead to a cardio respiratory arrest. If this downward spiral cannot be quickly reversed and stabilized with aggressive use of bronchodilators, steroids, nitrates, diuretics, or inotropes (depending upon the etiology) then ventilatory support is required to aid the fatiguing muscles of respiration.
It should be acknowledged that the act of intubation can be associated with substantial risks. These include the risks of sedative agents and neuromuscular blockers, difficult laryngoscopy with hypoxia or even complete loss of the airway, upper airway trauma, hypotension, and cardiac arrest. Prolonged intubation with mechanical ventilation is associated with barotrauma, nosocomial pneumonia, sinusitis, otitis, sepsis, tracheal stenosis, sedation-related problems and patient discomfort. There is a need for continuous, intensive monitoring which is costly and intubation itself will increase length of ICU stay (patients are often intubated for longer periods of time than necessary, with respirator weaning generally being performed only during day shifts). Because of the associated risks of intubation and mechanical ventilation, physicians have tended to delay the decision to intubate for as long as possible, in hopes that the patient will "turn around." One of the advantages of NIVS is that it can be easily applied and removed and thus used earlier in the course of acute respiratory failure.
The indications for intubation generally are a significant threat or compromise to any of the three "pillars" of the airway; (1)upper airway patency (airflow integrity), (2)protection from aspiration, or (3) significant compromise to oxygenation/ventilation. It is obvious that if either airway patency or protection is a problem then an endotracheal tube is required. However, a significant proportion of patients with compromise of oxygenation/ventilation have intact, patent upper airways and maintenance of protective airway reflexes. It is in this subset of patients where the use of Non-Invasive Ventilatory Support (NIVS) is becoming more prevalent. NIVS can be defined as any technique that increases alveolar ventilation and oxygenation without the placement of an endotracheal tube. The two most common modes of NIVS are Continuous Positive Airway Pressure (CPAP) and Bi-level Positive Airway Pressure (BiPAP). However, it should be kept in mind that NIVS is not an absolute substitute to intubation and has several limitations including lack of definitive control of the airway or definitive control of ventilation. There is no access for pulmonary toilet if there are significant respiratory tract secretions. It cannot be used in apneic patients. There is a need for patient cooperation. It can cause aerophagia. Facial skin necrosis can result from prolonged or improper use.
Mask CPAP works by assisting spontaneous ventilation and gas exchange. By maintaining a continuous positive airway pressure, CPAP recruits closed (atelectatic) alveoli and increases transpulmonary pressure and thus increases functional residual capacity (FRC) resulting in improved oxygenation. Increases in lung volume may improve lung compliance by shifting the compliance curve towards the elbow or steep portion. This will decrease work of breathing. By matching intrinsic PEEP the threshold load to initiating respiration is decreased. This also decreases work of breathing. In pulmonary edema it can decrease shunt and improve oxygenation by recruiting alveoli and redistributing lung water away from the alveolar gas exchange vessels. It can also decrease pulmonary edema by decreasing preload and afterload. In summary, CPAP can decrease the work of breathing and thus spare failing muscles of respiration, improve oxygenation, and also decrease preload and afterload to the heart.
Substantial advances in mask design have lead to improvements in mask fit, comfort, and dead space and have minimized air leaks. This has allowed higher airway pressures to be applied and resulted in much better patient tolerance. Either full face or nasal masks can be used. Mask CPAP is simple, cheap, and easy to use. All that is required is a high flow gas source ( > 50 LPM), a PEEP valve, tubing, and a facemask. Typically, a patient is started on 5 cm H2O pressure of CPAP with the oxygen concentration adjusted as necessary. The CPAP is increased in 2.5 cm H2O increments if necessary. However, as pressures are increased the negative hemodynamic consequences of positive pressure ventilation (decreased venous return with hypotension and decreased cardiac output) become more likely, as does the risk of hyperinflation and barotrauma. CPAP should probably not be increased above 10 cm H2O unless the treating physician has substantial experience with CPAP and mechanical ventilation.
Improvements in ventilator circuitry and sensing devices have also allowed NIVS to become more efficacious and better tolerated by patients. Newer ventilators are able to compensate for leaks inherent with facemasks, are able to generate higher flows than previously, and have improved trigger function so that they are more responsive to patient respiratory demands. All this results in improved patient-ventilator synchrony. With the development of the BiPAP Ventilatory Support System, we now have the ability to add positive pressure inspiratory support to CPAP and thus increase alveolar ventilation. This $8000 device is made by Respironics Inc. It is small, lightweight, readily portable and simple to learn to use. BiPAP ventilators cycle between two levels of positive airway pressure, with the higher level supporting ventilation during inspiration and the lower level maintaining airway patency during expiration. When the patient initiates a respiratory effort the BiPAP machine senses this and gives Inspiratory Positive Airway Pressure (IPAP) to facilitate inhalation. Upon the completion of inspiration, the device senses that exhalation is beginning and the amount of supportive pressure is automatically decreased so that patients do not have to exhale against the same pressure that supported inhalation. This Expiratory Positive Airway Pressure (EPAP) is analogous to PEEP or CPAP. Ordinarily, the patient maintains his own respiratory rate and pattern. Typical initial settings have the inspiratory support at 10cm H2O pressure and the expiratory support at 5cm H2O. The IPAP and EPAP pressures can be adjusted upward independently as necessary. Again, 2 to 3 cm H2O pressure increments are generally used. The EPAP level is set at least 5 below IPAP. Caution should be used if the EPAP is increased above 10 cm H2O as this is associated with greater patient intolerance (because of aerophagia) and a higher incidence of hemodynamic compromise. The maximal IPAP is 20 to 30 cm H2O depending upon the machine. Patients can be given inhalation therapy with adrenergic or other medications through the device. A beneficial effect is usually obvious by 20 to 40 minutes. If a patient is not improving by this time, then endotracheal intubation should be considered.
The indications for use of BiPAP are:
- Respiratory failure not requiring immediate intubation with:
- medically unacceptable or worsening alveolar hypoventilation
- acute respiratory acidosis
- ventilatory muscle dysfunction/fatigue (accessory muscle use or abdominal paradox)
- severe respiratory distress
- unacceptable hypoxemia despite supplemental oxygen
- Intubation contraindicated or refused
- Post-extubation respiratory difficulty in which reintubation may be avoided with a trial of BiPAP
The patient should be awake, alert, and cooperative with a patent upper airway, intact protective airway reflexes, and intact respiratory drive. Ideally, there should not be excessive respiratory secretions and the patient should be hemodynamically stable.
With regard to contraindications or relative contraindications to mask CPAP or BiPAP therapy, the following categories of patients have been defined:
- proper mask fit cannot be achieved, facial or nasal trauma
- excessive mask pressure requirements
- upper airway dysfunction
- cardiovascular instability
- upper GI bleeding
- excessive, unmanageable secretions
- uncooperative patients
- markedly depressed mental status or respiratory drive
Patients should be monitored closely for signs of barotrauma (pneumothorax/ pneumomediastinum) and for hypotension secondary to decreased venous return.
There are a substantial number of clinical trials concerning the efficacy of mask CPAP that can be used to defend the position that this therapy ought be developed into what is considered routine and expected treatment of acute respiratory insufficiency. The literature is particularly strong for its use in COPD and pulmonary edema. Successful use has also been reported with asthma, PCP pneumonia, neuromuscular weakness, post-operative respiratory distress, and traumatic lung contusions. The use of NIVS in acute respiratory failure is associated with prompt improvement in acid-base balance as determined by arterial blood gases obtained within the first few hours. Any patient with acute respiratory distress significant enough to result in more than mild accessory muscle use should be considered for this technique. Off-loading the respiratory muscles early in the presentation of acute respiratory failure, and supporting respiration while waiting for medical therapy (bronchodilators, steroids, antibiotics, diuretics, or nitrates) to have their effects, can potentially result in more rapid improvement and a lower incidence of intubation. All Emergency Departments should have rapid access to at least one mode of Non-invasive Ventilatory Support. If you do not have access to a BiPAP machine, mask ventilation can be easily accomplished using a standard ventilator by simply substituting a facemask for an endotracheal tube as the interface between patient and ventilator. However, for optimal performance, a later generation ventilator is required ( i.e., Puritan Bennett 7200, Siemans 900c, Siemans 300 ).
In summary, the use of NIVS should be considered early in the course of moderately severe acute respiratory failure. It is clear that use of NIVS is well tolerated and is associated with improved gas exchange and avoidance of intubation in appropriately selected patients with acute respiratory failure. It is simple and convenient to use, and has the potential to decrease both morbidity and costs when compared to standard invasive mechanical ventilation. Any patient with significant accessory muscle use, hypoxia, or respiratory acidosis could potentially benefit from its use. If you do not yet have easy access to CPAP or BiPAP in your Emergency Department, I would encourage to obtain it.
Mehta,S., et al : Randomized, Prospective Trial of Bilevel versus Continuous Positive Airway Pressure In Acute Pulmonary Edema. Crit Care Med 25:620, 1997.
Kramer, N, et al; Randomized, prospective trial of noninvasive positive pressure ventilation in acute respiratory failure. Am J Resp Crit Care Med 151:1799,1995.
Sacchetti,AD., et al : Bi-level positive pressure support system use in acute congestive heart failure:Preliminary case series. Acad Emerg Med 2:714, 1995.
Lin,M., et al : Reappraisal of continuous positive airway pressure in acute cardiogenic pulmonary edema:Short-term results and long-term follow-up. Chest 107:1379,1995.
De Lucas,p., et al : Nasal continuous positive airway pressure in patients with COPD in acute respiratory failure: A study of the immediate effects. Chest 104 :1694,1993.
Pennock,BE, et al : Noninvasive nasal mask ventilation for acute respiratory failure : Institution of a new therapeutic technology for routine use. Chest 105 : 441, 1994.
Holt,AW., et al; Intensive care costing methodology : Cost benefit analysis of mask continuous positive airway pressure for severe cardiogenic pulmonary oedema. Anaest Intens Care 22 : 170, 1994.
Pollack,Cv, et al; Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by nasal bilevel positive airway pressure circuit. Ann Emerg Med 26: 552, 1995.
Fortenberry,JD, et al; Management of pediatric acute hypoxemic respiratory insufficiency with bilevel positive pressure nasal mask ventilation. Chest 108: 1059, 1995.
Barbe,F, et al; Noninvasive ventilatory support does not facxilitate recovery in chronic obstructive pulmonary disease. Eur Resp J 9:1240,1996.
Bernstein, AD, et al; Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. NEJM 325 : 1825, 1991.
Petrof, BJ, et al; Continuous positive airway pressure reduces work of breathing and dyspnea during weaning from mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Resp Dis 141 : 281, 1990.
Ambrosino, N, et al; Physiologic evaluation of pressure support ventilation by nasal mask in patients with stable COPD. Chest 101 : 385, 1992.
Benhamou D, et al; Nasal mask ventilation in acute respiratory failure: Experience in elderly patients. Chest 102 ; 912,1992.
Brochard L, et al; Reversal of acute exacerbations of COPD by inspiratory assisstance with a face mask. NEJM 325: 1523, 1990.
Criner GJ, et al; Finanacial implications of noninvasive PPV. Chest 108; 475,1995.
Meduri GU, et al; Noninvasive positive pressure ventilation in status asthmaticus. Chest 110:767,1996.
Meduri GU, et al; Noninvasive positive pressure ventilation via face mask: First line intervention in patients with acute hypercapnic and hypoxemic respiratory failure. Chest 109: 179, 1996.
Meyer TJ, et al; Noninvasive positive pressure ventilation to treat respiratory failure. Ann Intern Med 120; 760, 1994.
Curreri JP, et al: Noninvasive positive pressure ventilation. What is its role in treating acute respiratory failure ? Postgraduate Med 99: 221, 1996.
Meyer TJ, et al; Noninvasive positive pressure ventilation to treat respiratory failure. Ann Intern Med 120: 760, 1994.
Patrick Melanson, MD, FRCPC