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Respiratory Intensive Care
Symposium on Intensive Care Units
Respiratory Intensive Care A. Gerald Shapiro, M.D.,* and Charles G. Walker, A.RLT.**
The survival rate of patients with acute respiratory failure, when treated in a unit specifically designed for their management, far exceeds the survival rate of these patients when treated in other forms of intensive care units. This reduced mortality rate admittedly requires adequate intermediate therapy (proper transportation, airway management, and artificial ventilation) as well as careful management in the intensive care unit. Furthermore, follow-up care must be considered, for the appropriate measures in the post intensive care phase can often make the difference between relapse and recovery. Although the scope of management must include the entire patient, physiological and clinical monitoring and respiratory therapeutics and pharmacologies must be recognized as the principal factors in the treatment of these patients.
RESPIRATORY FAILURE Respiratory failure results when the body's compensatory mechanism for alveolar hypo ventilation and associated hypoxia fail to meet physiological demands. Though respiratory failure may arise secondary to various disturbances, as outlined in Table 1, non-obstructive lung disease is the commonest cause.
Clinical Diagnosis The clinical diagnosis of ventilatory insufficiency may not be initially apparent and may require careful, constant observation for an hour or more. If the disease is progressive, the situation will soon become evident. Early in the process any of the following may be present: dyspnea, anxiety, weak cough with ineffective mucus clearing, difficulty in speaking because of dyspnea, fast and shallow respirations, the use of accessory muscles of respiration, flaring of alae nasi, tachycardia, "Director, Respiratory Therapy and Pulmonary Laboratory, The Valley Hospital, Ridgewood, New Jersey; Professor and Chairman, Respiratory Therapy Department, Alphonsus College, Wood cliff Lakes, New Jersey **Assistant Professor of Respiratory Therapy, Alphonsus College, Woodcliff Lakes, New Jersey
Medical Clinics of North America- Vol. 55, No. 5, September 1971
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Table 1.
GERALD SHAPIRO AND CHARLES G. WALKER
Disease States Leading to Respiratory Failure Impaired Ventilation
Chronic airway obstruction: emphysema, chronic bronchitis, chronic asthma Restrictive defects Decreased lung expansion: interstitial fibrosis, pleural effusion, pneumothorax, fibrothorax Limited thorax expansion: kyphoscoliosis, multiple rib fractures, thoracic surgery, spinal arthritis Decreased diaphragmatic movement: abdominal surgery, ascites, peritonitis, severe obesity Neuromuscular defects: poliomyelitis, Guillain-Barre syndrome, multiple sclerosis, myasthenia gravis, botulism, tetanus, brain or spinal injuries, drugs or toxic agents (curare, acetylcholinesterase inhibitors, polymyxin B and E, kanamycin, streptomycin, neomycin), amyotrophic lateral sclerosis, status epilepticus, polyneuritis, Landry's ascending paralysis Respiratory center damage or depression: narcotics, barbiturates, tranquilizers, anesthetics, cerebral infarction or trauma, prolonged therapy with a high oxygen concentration, post infectious encephalopathy.
Impaired Diffusion and Gas Exchange Pulmonary fibrosis: sarcoidosis, Hamman-Rich syndrome, pneumoconioses Pulmonary edema Cardiogenic Neuromuscular Obliterative pulmonary vascular disease: thromboembolism with blood, fat, bone marrow, or amniotic fluid Anatomic loss of functioning lung tissue: pneumonectomy, tumor
Ventilation-Perfusion Abnormalities and Venous Admixture Emphysema, chronic bronchitis, bronchiolitis, atelectasis, pneumonia, thromboembolism, post-perfusion syndrome, and congestive atelectasis
hypertension, dysphagia, headache, fatigue, and pale and cold, or flushed and warm, skin. As the course continues, the observer may note restlessness; severe anxiety and personality changes; insomnia (the patient will awaken with a start and find himself in greater respiratory distress); disorientation, dizziness, confusion, and unconsciousness; paradoxical respirations and the "rocking ship motion," which represents the activity of the diaphragm with intercostal muscle paralysis; cyanosis (provided no anemia exists); profuse diaphoresis; tracheal tug; flapping tremor; and miosis. These represent a combination of effects of the underlying disease and physiologic changes consequent to hypercapnea, hypoxia, and respiratory acidosis. Profound respiratory failure is associated with unconsciousness, tachycardia, gasping respirations, hypotension, and diaphoresis.
Methods of Detection of Ventilatory Failure The detection of ventilatory failure must be pursued in an organized fashion. The following may serve as a guide. 1. History, physical examination and clinical course. 2. Arterial pH usually decreases below 7.35 and is associated with a sharply rising arterial Peo2 of over 50 mm. Hg. If no supplemental oxygen is given, there is a progressively decreas-
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ing arterial P02 below 70 mm. Hg, and oxyhemoglobin de saturation. 3. A progressive rise in alveolar Pc02 , measured by the infrared method for the modified Haldane rebreathing technique, indicates ventilatory failure. When alveolar or arterial Pc02 reaches a critical level (80 to 90 mm. Hg, equivalent to 10 per cent CO 2 ) in a patient breathing room air, then there is insufficient alveolar oxygen to prevent arterial hypoxeInia and tissue hypoxia. 4. The determination of alveolar P0 2 /arterial P0 2 gradient provides an index to the degree of pulmonary ventilationperfusion abnormalities. 5. Measuring the vital capacity, besides being difficult, is not always accurate. Usually, the results represent the least that the patient can do and under these circumstances, a reduction of 60 to 70 per cent from the patient's approximate normal would indicate ventilatory need. On the other hand, the maximum mid-expiratory flow rate is a sensitive indicator of expiratory air flow obstruction, possibly more sensitive than the one-second forced expiratory volume deterInination, and is normally 2 to 10 liters per second. A 1 to 2liters per second value may be the only abnormality seen in an otherwise asymptomatic patient, but such a level is indicative of impending respiratory failure. This test is also very helpful in measuring bronchodilator response.
Constant skilled observation is an obvious requirement, and a skilled observer will not require a laboratory to know that a patient is in distress. It is difficult, however, to judge respiratory function and ventilatory need when the patient is unconscious, in shock, and acyanotic. Signs of respiratory insufficiency in the immediate postoperative patient are minimal and can be completely obscured by oversedation or residual anesthesia. Tachypnea and tachycardia may be indicative of other problems, and in such instances laboratory findings must be utilized. Determinations of arterial pH, Pc02 , standard and actual bicarbonate, total CO 2 , base excess, P02 , and oxygen saturation of hemoglobin, as well as alveolar Pc02 and P0 2 , must be readily available on a 24-hour basis.
AIRWAY MANAGEMENT Maintaining an airway is one of the most important aspects of the care of the patient with respiratory difficulty, and must be given the utmost priority. Often, proper airway management can spell the difference between success and failure, and any delay in implementation of the necessary procedures can result in untoward complications, not least of which is loss of life. Once the existence of airway obstruction, partial or complete, has been established, an immediate hyperextension of the head and flexion of the neck may clear hypopharangeal obstruction caused by relaxation of the base of the tongue. Positive pressure inflation attempts should next be made in order to establish the effectivenesss of this maneuver, as well as to establish initial gas exchange. Clearing of the oropharynx will be necessary to prevent further obstruction and aspiration of foreign material. Forward displacement of the mandible is indicated to further eliminate physiological obstruction, and insertion of an oropharyngeal airway may be necessary. If these procedures are not successful in establishing a patent airway, or if the recovery of normal physiologic airway patency is not expected immediately, endotracheal intubation must be done. Using nasotracheal suction and an oropharyngeal airway for more than a short period of time carries potential hazards. Endotracheal intubation should therefore be considered from the outset in patients in whom manage-
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ment of secretions, the inability to insure a patent airway, or the possible need for mechanical ventilation exists. Eventual tracheostomy must be considered to insure the patency of the airway in patients in whom respiratory failure and a pending respiratory crisis coexist with difficulty in the management of secretions. Tracheostomy should never be considered an emergency procedure but rather an elective, supportive measure. According to different authors, an endotracheal tube may be left in from a few days to 2 to 3 weeks, and this adequately supports the concept of intubation before, and often instead of, tracheostomy. Access to the lower part of the airway for the purpose of removing secretions can be achieved with endotracheal tube and tracheostomy alike, technique being the major difference. Problems with endotracheal tube cuffs, often used to justify tracheostomy, are not unique, for tracheostomy tubes can create similar difficulties. Table 2 lists advantages and disadvantages of nasotracheal intubation and tracheostomy. A clinical evaluation of the individual patient will be more valuable than any discussion in determining which procedure to use.
Endotracheal Tube Once the patient has been intubated, it is necessary to confirm the position of the tracheal tube, initially through the use of a stethoscope, and later by roentgenographic examination. The tube must then be
Table 2. Advantages and Disadvantages of Nasal Endotracheal Intubation and Tracheostomy NASAL ENDOTRACHEAL TUBE
TRACHEOSTOMY
EITHER
Advantages Less interference with swallowing Easier and safer for prolonged use Easier to suction airway
Improves removal of secretions Facilitates connection of airway to respirators Reduces dead space
Esophageal compression
Infection of site
Swallowing is difficult
Bacterial contamination of airway Bleeding from trachea, carotid artery, or jugular vein Mediastinal emphysema
Obstruction of tube if inflated cuff slips Humidification and warming lost Bronchorrhea
Less interruption of body defenses Easily inserted and removed
Disadvantages
Speech is impossible May occlude one major bronchus Vocal cord damage
Harder to repeat
Kinking of tube
Extubation may be difficult
Subglottic edema
Narrow tube may not permit complete expiration so that venous return is impeded Tracheal necrosis from tube or inflated cuff Subsequent tracheal granuloma or stenosis
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secured in place with proper surgical adhesive tape, so that movement of the patient or of equipment attached to the tube does not dislodge it and cause its further movement into the right mainstem bronchus. If supportive oxygen therapy is considered at the onset, rather than mechanical ventilation, the oxygen cannula should never be placed directly into the endotracheal tube lumen. Such a catheter would reduce the size of the lumen and cause an increase in the resistance to exhalation, which is equivalent to an increase in the patient's work of breathing. Resistance to flow varies as the fourth power of the radius of a tube, so that even a slight decrease in the lumen will cause a great increase in resistance. Instead, a T-shaped adaptor may be constructed, or one of the many on the market may be used, to connect the oxygen cannula. An oxygen reservoir to increase concentration can be added to this type of adaptor, as well as increased dead space in the exhalation phase. Endotracheal suction must then be instituted immediately, as the patient no longer has the ability to cough. Large, low-pressure tracheal tube cuffs are indicated instead of small, narrow, high-pressure cuffs when artificial ventilation is required. The narrow cuff tends to increase the pressure on the tracheal wall over a small area, whereas the large, low-pressure cuff distributes a lower pressure over a wider area and tends to cause less trauma to the tracheal wall initially. However, tracheal trauma is still possible with the use of any cuff. Orotracheal Versus Nasotracheal Tubes An orotracheal tube may be used for 2 or 3 days, at which time the patient should be changed to a nasotracheal tube before the orotracheal tube can cause glottic trauma. A nasotracheal tube is easier to secure, can be tolerated well by the conscious patient, and can be used for 2 to 4 weeks, with proper supportive care. The nasotracheal tube does not irritate the tracheal mucosa as seriously as the orotracheal tube does. A major disadvantage of the nasotracheal tube is the limitation of its size by the size of the nasal opening. Tracheostomy Care The following are necessary at the bedside: Professionals trained in the care and management of the airway: a respiratory therapist or a nurse trained in airway management or both. Suction apparatus capable of achieving a vacuum equal to 120 mm. Hg. Sterile suction setup. Sterile tracheostomy dilators, or sterile Kelly clamp. Two spare tracheostomy tubes, one of the same size and one of the next smaller size, taped onto the wall above the patient's head. Humidification apparatus capable of producing 100 per cent water vapor saturation at body temperature. Endotracheal tube tray, complete and ready for use if the tracheostomy tube becomes dislodged. Good lighting. Complete, manual, self-inflating resuscitation bag, including mask and all adaptors necessary for endotracheal as well as tracheostomy tubes. A means of assessing ventilation. Pencil and paper for the conscious patient to use in communication.
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Complications of Tracheostomy The rewards of immediate or early tracheostomy are obvious, but they certainly must be weighed against the possibilities of complications. There is no ideal tracheostomy tube, and the associated complications can run the gamut from too great a delay in consideration to total obstruction of the tube, leading to asphyxiation. Each complication, therefore, is related to a specific course of action. Because of the limitation of space, these complications will only be listed.
Death. Pneumothorax, if the pleural spaces are entered. Cuff dislodgement, if the cuff on the tracheal tube slides down the barrel of the tube and occludes the distal orifice. Tracheal hemorrhage. Over-inflation of the cuff may compress the lumen of a soft tracheostomy tube. Tracheal erosion. Tracheopleural fistula. Tracheal stenosis. Tracheal dilatation. Dysphagia. Aspiration can occur in the presence of an uncuffed tracheostomy tube. Erosion of the innominate artery posteriorly. Tracheomalacia. Atelectasis may be caused by improper placement of the distal tip of the tracheostomy tube, into a major bronchus (usually the right bronchus). Improper suctioning leads to hypoxia, arrhythmia, and infection. U se sterile procedures at all times! Ineffective cuff pressure. The pressure within the balloon should not be allowed to exceed the capillary pressure. A stopcock and a manometer may be used to monitor the pressure within the tracheostomy balloon. Proper cuff inflation can be insured by inflating the cuff until a seal exists, and then backing off until there is a small leak of air audible through a stethoscope placed just superior to the tracheostomy wound. Pneumothorax related to positive pressure ventilation is overrated. It requires 80 cm. of pressure to rupture a lung out of the thorax, and considerably more when a lung is restricted by the thorax. Children are an exception. Infection secondary to respiratory therapy apparatus. Oxygen toxicity. Monitor oxygen content and titrate supplemental oxygen against increases in arterial P02 values. It is not considered necessary to maintain arterial oxygen partial pressure above 100 mm. Hg. Cardiac arrhythmia. 77 per cent of patients on ventilators have transient cardiac arrhythmias with a consequent increased mortality. These may be due to acidosis, hypoxia, electrolyte imbalance, or cardiotonic drugs. Inability to wean the patient from the ventilator. Apnea. Subcutaneous emphysema or mediastinal emphysema. Tension pneumothorax. Air embolism. Dislodging of tube. Wound infection, essentially a nursing problem reduced by education in proper techniques and precautions. Tracheal ulceration. Tracheitis. Blockage of endotracheal tube. Laryngotracheal bronchitis.
Standard Tracheostomy Care Doctors must complete and sign a standard order sheet for tracheostomy care or else must write detailed instructions. Where there is any doubt, or unless otherwise specified, nurses and respiratory therapists will follow standard procedures.
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Humidification is required on all tracheostomy patients. Patients who require more care than the usual irrigation and aspiration should be placed in the respiratory intensive care unit (e.g., those requiring ventilatory assistance). Nurses or respiratory therapists may remove the inner cannula of a metal tube for cleaning, but only physicians may change the outer cannula of a metal tracheostomy tube. The obturator, in a sterile pack, must be taped to the head of the bed, or on the chest wall. If the outer cannula is unexpectedly expelled, a nurse will remain with the patient and attempt to ventilate the patient through his nose and mouth, or through the tracheostomy opening. An aide is to summon medical aid. When a patient is on continuous ventilation, the cuff of the tube is to be deflated by the respiratory therapist (1) every hour for 5 minutes, with provisions made to compensate for the air leak; suctioning must accompany all deflation procedures; and (2) if the patient has difficulty in swallowing during meals. If a patient is to be discharged from the hospital with a tracheostomy tube in place, the teaching of the patient (and his family) should begin as soon as his condition warrants before his discharge. Decannulation must be specifically ordered in detail by the physician.
OXYGEN THERAPY With rare exceptions, oxygen should never be denied to a patient who exhibits the need for it on the basis of arterial blood gas analysis, nor should it ever be administered indiscriminately or without proper monitoring. The use of oxygen in the cardiopulmonary or respiratory emergency without due regard for the fractional inspired concentration of oxygen (F10 2 ) is considered acceptable. However, for routine therapy, or once the patient has been stabilized, a great deal of consideration must be given to maintaining the arterial P0 2 around the desired level of 100 mm. Hg. An important consideration in the administration of supplemental oxygen to a patient in acute respiratory failure is the relegation of his breathing stimulus to the peripheral chemoreceptors by a low arterial oxygen tension. Serious depression of ventilation can ensue when the patient influenced by this hypoxic drive is presented with an F 1 0 2 sufficient to reduce the stimulus to breathe. In this type of patient, an increase in the F 1 0 2 by 4 to 6 per cent will generally double the oxygen supply to the tissue. It will limit the rise of Pco 2 and avoid narcosis, ineffective cough, shallow breathing, and deterioration of the lung function. According to Campbell, small increments of inspired oxygen flows, 1 to 4liters per minute (24 to 32 per cent) have proved sufficient in obstructive lung disease, and efforts should be made to avoid higher concentrations. More ambitious methods, such as intermittent positive pressure breathing, may reduce cardiac output, reduce Pco 2 (or H+), and cause cerebral vasoconstriction, a shift of the oxygen dissociation curve to the left, and reduce the cerebral oxygen supply, even if the arterial P0 2 and saturation are normal. Any sudden fall in P0 2 under these circumstances is particularly disastrous.
Humidification Humidification of the oxygen, or any inspired gas, is absolutely mandatory, regardless of the form of delivery. Optimally, air reaching
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the carina should be at 100 per cent relative humidity at body temperature, especially in the case of tracheostomy or endotracheal intubation. Bubble-type humidifiers force a stream of oxygen through a layer of water to add water vapor to the dry gas by evaporation. A shortcoming of this type of humidifier is that water at room temperature is cooled by the evaporation process and therefore lowers the temperature of the gas that passes through it. Cooling decreases the moisture carrying capacity of the gas to allow only about 40 per cent relative humidity. Bubble-type humidifiers are used with small-bore tubing and are employed only for short-term, emergency therapy. They are absolutely inadequate to treat patients with tracheostomies or endotracheal tubes, although they may be used when the patient is receiving oxygen through a cannula or mask and thereby utilizing physiologic humidification mechanisms. Nebulizers use a gas stream, or electronic energy, to break a liquid into small particles, delivering water in droplet form as well as vapor. These droplets form a mist which represents gas supersaturated with water. Heating the water within the nebulizer chamber to well above body temperature, to allow for cooling during its delivery to the patient, usually will result in a relative humidity of 100 per cent at body temperature. Oxygen that is humidified by a nebulizer must be administered through a large-bore connecting tube, as the "rain-out" in a smaller tube, due to cooling, would soon obstruct it. Although heated humidifiers are generally indicated for the patient with a tracheostomy, it is well to withhold heat for the first 12 hours in order not to aggravate local bleeding at the site of the wound.
Hazards of Humidification Cold mist may increase metabolic demands by causing shivering. A heated nebulizer may interfere with heat loss and lead to elevated temperature, increased oxygen consumption, and eventually, an inTable 3. Complications of Therapy for Respiratory Failure Shock (50 per cent or more) Circulatory Septicemic Hypoxia and bradypnea Depression of ventilation Administration of oxygen Administration of narcotics and sedatives Extreme CO2 retention without O2 administration Ventilatory dysfunction Errors of airway management Infections (pulmonary) Oxygen toxicity Wet lung syndrome Gastrointestinal bleeding (10 to 15 per cent) and gastric dilatation Pulmonary embolism (5 to 10 per cent) Pulmonary-renal syndromes Acid-base or metabolic disturbances Arrhythmias Acute pancreatitis
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creased cardiac workload. Positive water balance and increased absorption may lead to overhydration and increased cardiac workload. Finally, humidification can be a potential source of infection - prolonged ultrasonic nebulizer therapy with normal saline may cause bronchopneumonia, loss of surfactant, atelectasis, protein exudate, and cell fragmentation of the epithelium.
Oxygen Toxicity No patient should receive more than 40 per cent oxygen, unless the arterial oxygen tension is less than 60 mm. Hg. Although no patient with hypoxia should ever be denied oxygen, its administration should be accurately and frequently monitored. The Bird "Mark 7," which is described as a "pressure generator" ventilator, is powered by compressed oxygen. The air mix control allows a mixture of gases to take place. However, the concentration of oxygen administered depends on the patient's ventilatory compliance and on the resistance to flow created by the tubing. At high pressure settings, the mechanism may malfunction, and high concentrations of oxygen may be delivered to the patient. Even with the Bird parallel inspiratory flow-mixing cartridges, the actual oxygen concentration delivered often cannot be determined by the settings alone. The higher the FIO z, the greater the toxic effects of oxygen that can be seen. Toxic effects are related to the loss of the lung's normal surface tension. Unfortunately, the pathophysiology develops long before the clinical picture when high oxygen concentrations are used. Decreasing arterial oxygen tension, necessitating an increased inspiratory oxygen concentration, should make one immediately suspect oxygen toxicity. A chest radiograph shows collapse and consolidation of the lungs. There is also an increase in ventilatory pressure with a dissociated decrease in minute ventilation Cif a volume-regulated respirator is used). Diffuse rales can be heard upon auscultation. To prevent oxygen toxicity, high concentrations of oxygen should not be administered for more than 24 to 36 hours. Arterial oxygen tension and the percentage of inspired oxygen should be monitored to maintain an arterial oxygen tension of 70 to 80 mm. Hg, or possibly 100 mm. Hg if a patient's cardiac output is good. However, if the alveolar arterial oxygen tension gradient exceeds 500 mm. Hg, continuous positive pressure ventilation should be considered. Caution must be used in the severely emphysematous patient and extreme lung volumes must be avoided. Oxygen toxicity is related to the loss of elasticity of the lungs. When the chest is opened in such a patient, no collapse of the lung is evident. The first phase is the hemorrhagic exudative stage where surfactant activity is impaired. The lungs become beefy and edematous. There are hyaline deposits, thickening of the alveolar walls, clear fluid material associated with pulmonary edema, destruction of the bronchioles, and emphysematous changes., The patient's behavior in such a manner imitates chronic obstructive lung disease, and he needs higher ventilatory pressures. The next phase is the proliferative phase a cellular fibrotic state. Increase of normal alveolar fibroblastic proliferation, a tufting of the
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capillary bed, outpouching of the alveolus, cellular proliferation, and eventually a stiff lung are the characteristics. Both phases can exist concurrently. There is a small elevation in the P aC02, which is normally harmless but has been known to aggravate the toxic effects of oxygen. Oxygen toxicity will also produce an x-ray picture of a decrease in compliance, associated with minimal aspiratable secretions and an eventual deterioration of blood gas values. There are no contraindications for oxygen therapy, but rather specific indications as governed by precautions.
INDICATIONS FOR VENTILATION The most common indication for controlled ventilation is respiratory insufficiency. Assisted ventilation may be used for any condition in which respiratory activity is either completely absent or, if present, is insufficient to maintain either adequate oxygenation or carbon dioxide clearance. It has been suggested that acute respiratory failure is present and deserving of intensive therapy if there is clinical evidence for it supported by findings of an arterial blood pH less than 7.25, arterial blood carbon dioxide tension greater than 55 mm. Hg, or an arterial blood oxygen tension less than 60 mm. Hg. Such data are more significant if they represent an acute change. Patients in respiratory insufficiency (an acutely elevated P aC02 without pH changes, with or without hypoxemia) or who are in impending respiratory insufficiency (e.g., a chronic asthmatic) should be considered candidates for ventilatory therapy too. Generally, the more rapid the deterioration and the healthier the patient before the exacerbation of the acute illness, the more likely it is that the patient will require assisted ventilation. Arterial pH and blood gas levels are useful guidelines to indicate the need for mechanical ventilation, provided that they are not used as absolutes to initiate action. Some patients with chronic pulmonary disease have a P aC02 above 50 mm. Hg but are not in respiratory failure. Patients with chronic metabolic acidosis have a low P aC02 and would be considered to be in respiratory failure if the Pco 2 were elevated. Pneumothorax without chest tubes, hemorrhagic shock, inadequate functioning of lung tissue, and unskilled personnel may be contraindications to mechanical ventilation. The Use of Ventilators In considering the mode of operation of any ventilator, it is necessary to distinguish four functions. The ventilator must inflate the patient's lungs, deflate the lungs (or allow passive expiration), have some means to "decide" when to stop inflation and start expiration, and some other means by which it "decides" when to stop expiration and start inflation again (Asmundsson). The ventilator should include at least the following characteristics: Capability of operating for long periods with a minimum of servicing and a maximum freedom from the risk of mechanical breakdown.
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Provisions for operating the instrument on room air, pure oxygen, a variable mixture of both, and any other gas desired. Dependable control over the generated pressure, whether the ventilator is pressure generated or volume generated. Variable flow control, either manual or automatic. Control of frequency. A combination of both control and assistive capabilities for greater versatility in handling the changing patterns of breathing. Negative pressure during exhalation for the patient undergoing prolonged controlled ventilation. Provisions for adequate humidification of inspired air. A means of adjusting the inspiratory-to-expiratory time ratio, or at best a provision to insure that inspiration does not exceed expiration. Some means to monitor delivered tidal volume and airway pressure. A sigh mechanism.
MONITORING Once the medical team, through the use of a mechanical ventilator, assumes a life-support function for the patient, adequate means must be established to judge the continuing effectiveness of this therapy. It is no longer enough to assess the patient's ventilatory needs by clinical observation of signs and symptoms alone. Nor is it desirable to interpret physiologic data such as that determined by blood gas analysis without consideration of a well documented clinical picture. Technological progress in the development of electronic and mechanical monitoring devices has allowed the assessment of many physiological parameters and mechanical functions. The best approach to evaluation of respiratory therapy combines the use of such devices with careful clinical observation by well-trained personnel. Even with the best care and monitoring, therapy for respiratory failure is plagued with complications (Table 3).
Clinical Monitoring Close clinical observation of the patient being maintained on mechanical ventilation is mandatory. The interpretation of signs and symptoms, based on an understanding of the physiology of the disease states responsible for the aberration of ventilatory function, can often spell the difference between averting a problem and having to treat its result. Routine auscultation of the chest is a valuable means of assessing airway patency as well as ventilatory distribution. Proper placement of an endotracheal or tracheostomy tube must also be confirmed by auscultation. The need for suctioning can be ascertained well in advance of associated compliance changes. Observation of the patient's diaphragmatic excursion and changes in the use of accessory muscles of breathing can signal an inefficiency of effort, or an increase in the work of breathing. Paradoxical movements of the epigastrium as well as distention of the abdomen may signal early complications of therapy. Cyanosis, although not a reliable sign of hypoxia, may give notice of an acute ventilation perfusion abnormality. Changes in peripheral
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circulation will also be associated with notable changes in the color of the skin. To assure adequate ventilation in certain disease states, it may also become necessary to alter the inspiratory/expiratory ratio to a point where an increase in the mean intrathoracic pressure eventually results in decreased cardiac output. Although this condition is generallyassociated with inspiratory/expiratory ratios below 1: 1, it is a consideration in any patient in whom positive pressure respiration is employed on a continuous basis. Physiologic (Analytical) Monitoring Physiologic or analytical monitoring should serve not as an alternative to continual clinical evaluation, but rather as an adjunct. An arterial blood sample should be drawn as close to the onset of the ventilatory crisis as possible - preferably prior to the institution of mechanical ventilation. This is often impossible, however, and should be deferred in situations where prompt treatment is necessary. Arterial blood gas determinations should be made within the first 10 to 15 minutes following start of mechanical ventilation. Adjustments can then be made in oxygen concentration, respiratory frequency, and tidal volume, in order to approximate the desired blood gas and acid base status. Repeated blood gas analysis every half hour (or more frequently) may well be necessary until the patient's clinical and physiologic status become stable. A patient's acid-base status may be returned to normal, generally at a rate which does not exceed that rate at which the abnormality manifested itself. A general rule of thumb concerning the return of partial pressure of carbon dioxide when accompanied by a pH change is that the P a co 2 may be lowered at a rate of approximately 10 mm. Hg per hour. This is relative and is open for interpretation on an individual basis. Great care must be taken when compensatory pH changes exist in the face of elevated carbon dioxide levels. Overzealous ventilation of this type of patient can often result in an overwhelming alkalosis. The partial pressure of arterial oxygen should be maintained within the 80 to 100 mm. Hg range. One of the drawbacks of arterial blood gas analysis has been the unavailability of attending physicians or house staff members for drawing the arterial sample. Although the decision for blood gas analysis must originate with the physician, the actual drawing of the sample can certainly be relegated to the trained respiratory therapist, a practice which has received wide attention of late. In order to stabilize the patient during the acute period, repetitive arterial sampling is usually necessary, and utilization of an indwelling arterial cannula may be considered. The insertion of an indwelling arterial catheter is a technique which should be reserved for the physician. Once a "physiological equilibrium" exists between the patient and the mechanical ventilator, and the patient can be considered stable, blood gas analysis need only be done 2 or 3 times each day. Standing orders for arterial blood gas analysis, indicating frequency, are essential. This allows the respiratory therapist or nurse to report not only the clinical situation but also the resultant physiological changes.
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In the patient in whom repeated arterial blood gas analysis is necessary, the use of the arterialized capillary sampling technique may provide an alternative. A micro sample of approximately 50 to 150 micro liters of blood is obtained from the selected site (usually the heel of the hand) after "arterializing" the area through the use of wet heat. The sample is analyzed using routine blood gas analysis techniques. Within normal physiological ranges, this technique closely approximates arterial blood gas analysis. Inaccuracies, however, are associated with the higher physiological ranges. Proper technique is essential for reliable results. The use of venous blood as an assessment of ventilatory status is not accurate, as venous blood is generally considered to reflect the tissue status of that area served by the vein selected for sample. The use of central venous blood and its correlation to arterial blood for Pc02 and pH de terminations has been discussed in recent years. In view of the difficulty in assessing the exact placement of a central venous catheter and the inability to correlate oxygen tension, it is the opinion of the authors that this method is not a reasonable alternative to arterial blood gas determination. The rebreathing technique for determining alveolar Pco2 has been shown to have direct correlation with arterial Pco2 • This method is useful for evaluating the effectiveness of alveolar ventilation, particularly when monitoring the patient in the non-acute phase. Other Monitoring Techniques Advances in technology have placed additional techniques and valuable information at the disposal of the management team. Electrocardiographic monitoring should be employed for those patients receiving augmented ventilatory support. Blood pressure, intravenous infusion rate, and respiratory rate can also be monitored electronically. Indwelling arterial blood gas electrodes make possible the continuous surveillance of blood gas status, although their use is still limited and in need of more clinical evaluation. The use of indwelling electrodes combined with expiratory gas sampling, and information gained through the use of expiratory pneumotachographic information, have made possible a continuous on-line computerized analysis of a patient's ventilatory status. Monitoring Equipment Function One of the most important considerations in assuring the success of assisted mechanical ventilation is constant surveillance of the ventilator's function, as well as the manner in which the technical aspects of ventilation are managed. All too often, situations such as "plumbing accidents," mechanical disconnections, or even failure of the management team to interpret properly the patient's status can compromise the patient's status beyond our ability to assist him. A mechanical ventilator which is being used to duplicate the mechanical and physiologic function of breathing, in addition to being in c~nstant attendance by a knowledgeable technician, should be equipped with a device that will signal disconnection. An audiovisual alarm system is the most appropriate method.
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The exhaled tidal volume should be able to be observed breath by breath. With the appearance of electronic equipment for this function, the use of positive displacement spirometers has waned; yet a great deal of information can be gained through the use of these devices. For example, slowed expiratory flow rates are easily visible on a positive displacement spirometer, whereas they may not be immediately visible through an electronic device. A mechanism to establish effectively the inspired oxygen content must also be present, and an audiovisual alarm may also be an asset. A manometer which enables the operator to determine the delivery pressure of the system is important in the monitoring scope of a ventilator. Also helpful are means whereby the inspiratory/expiratory ratio can be obtained, as well as a method to approximate compliance. This can be accomplished through tidal volume and pressure monitors. To assist in monitoring both the management and the technical aspects of ventilatory assistance, we have designed three basic flow sheets. The first is placed on the ventilator and is used for recording the initial settings of the ventilator. This sheet is kept on the ventilator, and subsequent changes placed on the sheet alert all personnel of authorized changes in settings. The second flow sheet, the "Sequential Blood Gas Data Record," is placed on the patient's chart. All blood gas data, in chronological order, are logged on this record, along with therapeutic measures which may cause subsequent alterations. This record, of course, correlates directly with the first flow sheet, in that it provides justification for changes in settings. The third sheet is a respiratory care record on which the respiratory therapist or nurse records all data relative to the ventilatory status of the patient. Medicolegal considerations make the recording and retrieval of this type of data important.
REFERENCES Amberson, J. B.: The management of acute respiratory failure in chronic bronchitis and emphysema. Amer. Rev. Resp. Dis., 96:626,1967. American Thoracic Society, Committee on Therapy: Therapy of acute respiratory failure. Amer. Rev. Resp. Dis., 93:3, 1966. Asmundsson, T., et a!.: Complications of acute respiratory failure. Ann. Intern. Med., 70: 484,1969. Bates, D. V., Macklem, P. T. and Christie, R. v.: Respiratory Function in Disease. 2nd ed. Philadelphia, W. B. Saunders Company, 1971. Belinkoff, S.: Introduction to Inhalation Therapy. Boston, Little, Brown & Co., 1969. Bendixon, H. H.: Respiratory Care. St. Louis, C. V. Mosby Co., 1965. Birley, D. M., et al.: The place of the intensive therapy unit in the general hospital. Acta Anaesth. Scandinav., vol. 23, suppl. 92, 1966. Campbell, D.: Four years of respiratory intensive care. Brit. Med. J., 4:255,1969. Comroe, J. H., et a!.: The Lung. 2nd ed. Chicago, Yearbook Medical Publishers, 1962. Dines, D. E., et al.: Monitoring certain aspects of respiratory failure. Dis. Chest, 54:421, 1968. Egan, D. C.: Fundamentals of Inhalation Therapy. St. Louis, C. V. Mosby Co., 1969. Feldman, S. A.: Tracheostomy and Artificial Ventilation. Baltimore, Williams & Wilkins, 1967. Handbook of Physiology, Section III (Respiration), vols. 1 and 2. Washington, American Physiological Society, 1964-1965. Hayman, L. D.: Policies and procedures of an intensive care unit. North Carolina Med. J.. 1968, p. 250. Kibelstis, J. A.: Management of respiratory failure. AFP/GP, 2:90,1970. Mushin, W. W., et al.: Automatic Ventilation of the Lung. 2nd ed. Oxford, Blackwell Scientific Publishers, 1969. Noehren, T. H., et al.: The ventilation unit for special intensive care of·patients with respiratory failure. J.A.M.A., 203:641, 1968.
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O'Donohue, W. J., Jr., et al.: The management of acute respiratory failure in an RICU. Chest, 56:603, 1970. Petty, T. L.: P.S. Don't forget the respiratory intensive care unit. Dis. Chest, 56:276, 1969. Petty, T. L., et al.: Management of acute respiratory failure (a systemic approach). Ann. Allergy, 26:405, 1968. Petty, T. L., et al.: The intensive respiratory care unit. California Med., 107:381, 1967. Petty, T. L., et al.: Comprehensive care program for airway obstruction. Ann. Intern. Med., 70:1109,1969. Ramachandran, P. R., et al.: Changes in functional residual capacity during respiratory failure. Canad. Anaesth. Soc. J., 17:359, 1970. Rogers, R. M.: Respiratory insufficiency: Treatment with mechanical ventilators. Medical Times, 98:197,1970. Safar, P.: Respiratory Therapy. Philadelphia, F. A. Davis Co., 1965. Segal, M. S.: Treatment of acute respiratory failure. New Eng. J. Med., 274:841,1966. Shelley, M. K.: Acid-base measurements in intensive care. Biomed. Sci. Instrum., 5:41, 1969. Stone, D. T.: Management of ventilation failure. New York State J. Med., 1970. Sykes, M. K.: Accessories for humidifiers. Anaesthesia, 22:668, 1967. Tse, R. L., and Lee, M. W.: pH of infusion fluids. J.A.M.A., 215:642,1971. Tysinger, D. S.: The place of respiration in the coronary care unit. J. Med. Assoc. State of Alabama, 39:355, 1969. Wagner, W. W., Jr., et al.: Pulmonary gas transport time: Larynx to alveolus. Science, 163: 1210, 1969. Warrell, D. A., et al.: Effects of controlled oxygen therapy on arterial blood gases in acute respiratory failure. Brit. Med. J., 2:452, 1970. Whipple, H. E., ed.: Respiratory failure. Ann. N.Y. Acad. Sci., 121 :651, 1965. Winter, P. M., et al.: Acute respiratory failure. Scientific American, 221 :23,1969. Valley Hospital Ridgewood, New Jersey 07450
Respiratory Intensive Care A. Gerald Shapiro, M.D.,* and Charles G. Walker, A.RLT.**
The survival rate of patients with acute respiratory failure, when treated in a unit specifically designed for their management, far exceeds the survival rate of these patients when treated in other forms of intensive care units. This reduced mortality rate admittedly requires adequate intermediate therapy (proper transportation, airway management, and artificial ventilation) as well as careful management in the intensive care unit. Furthermore, follow-up care must be considered, for the appropriate measures in the post intensive care phase can often make the difference between relapse and recovery. Although the scope of management must include the entire patient, physiological and clinical monitoring and respiratory therapeutics and pharmacologies must be recognized as the principal factors in the treatment of these patients.
RESPIRATORY FAILURE Respiratory failure results when the body's compensatory mechanism for alveolar hypo ventilation and associated hypoxia fail to meet physiological demands. Though respiratory failure may arise secondary to various disturbances, as outlined in Table 1, non-obstructive lung disease is the commonest cause.
Clinical Diagnosis The clinical diagnosis of ventilatory insufficiency may not be initially apparent and may require careful, constant observation for an hour or more. If the disease is progressive, the situation will soon become evident. Early in the process any of the following may be present: dyspnea, anxiety, weak cough with ineffective mucus clearing, difficulty in speaking because of dyspnea, fast and shallow respirations, the use of accessory muscles of respiration, flaring of alae nasi, tachycardia, "Director, Respiratory Therapy and Pulmonary Laboratory, The Valley Hospital, Ridgewood, New Jersey; Professor and Chairman, Respiratory Therapy Department, Alphonsus College, Wood cliff Lakes, New Jersey **Assistant Professor of Respiratory Therapy, Alphonsus College, Woodcliff Lakes, New Jersey
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Table 1.
GERALD SHAPIRO AND CHARLES G. WALKER
Disease States Leading to Respiratory Failure Impaired Ventilation
Chronic airway obstruction: emphysema, chronic bronchitis, chronic asthma Restrictive defects Decreased lung expansion: interstitial fibrosis, pleural effusion, pneumothorax, fibrothorax Limited thorax expansion: kyphoscoliosis, multiple rib fractures, thoracic surgery, spinal arthritis Decreased diaphragmatic movement: abdominal surgery, ascites, peritonitis, severe obesity Neuromuscular defects: poliomyelitis, Guillain-Barre syndrome, multiple sclerosis, myasthenia gravis, botulism, tetanus, brain or spinal injuries, drugs or toxic agents (curare, acetylcholinesterase inhibitors, polymyxin B and E, kanamycin, streptomycin, neomycin), amyotrophic lateral sclerosis, status epilepticus, polyneuritis, Landry's ascending paralysis Respiratory center damage or depression: narcotics, barbiturates, tranquilizers, anesthetics, cerebral infarction or trauma, prolonged therapy with a high oxygen concentration, post infectious encephalopathy.
Impaired Diffusion and Gas Exchange Pulmonary fibrosis: sarcoidosis, Hamman-Rich syndrome, pneumoconioses Pulmonary edema Cardiogenic Neuromuscular Obliterative pulmonary vascular disease: thromboembolism with blood, fat, bone marrow, or amniotic fluid Anatomic loss of functioning lung tissue: pneumonectomy, tumor
Ventilation-Perfusion Abnormalities and Venous Admixture Emphysema, chronic bronchitis, bronchiolitis, atelectasis, pneumonia, thromboembolism, post-perfusion syndrome, and congestive atelectasis
hypertension, dysphagia, headache, fatigue, and pale and cold, or flushed and warm, skin. As the course continues, the observer may note restlessness; severe anxiety and personality changes; insomnia (the patient will awaken with a start and find himself in greater respiratory distress); disorientation, dizziness, confusion, and unconsciousness; paradoxical respirations and the "rocking ship motion," which represents the activity of the diaphragm with intercostal muscle paralysis; cyanosis (provided no anemia exists); profuse diaphoresis; tracheal tug; flapping tremor; and miosis. These represent a combination of effects of the underlying disease and physiologic changes consequent to hypercapnea, hypoxia, and respiratory acidosis. Profound respiratory failure is associated with unconsciousness, tachycardia, gasping respirations, hypotension, and diaphoresis.
Methods of Detection of Ventilatory Failure The detection of ventilatory failure must be pursued in an organized fashion. The following may serve as a guide. 1. History, physical examination and clinical course. 2. Arterial pH usually decreases below 7.35 and is associated with a sharply rising arterial Peo2 of over 50 mm. Hg. If no supplemental oxygen is given, there is a progressively decreas-
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ing arterial P02 below 70 mm. Hg, and oxyhemoglobin de saturation. 3. A progressive rise in alveolar Pc02 , measured by the infrared method for the modified Haldane rebreathing technique, indicates ventilatory failure. When alveolar or arterial Pc02 reaches a critical level (80 to 90 mm. Hg, equivalent to 10 per cent CO 2 ) in a patient breathing room air, then there is insufficient alveolar oxygen to prevent arterial hypoxeInia and tissue hypoxia. 4. The determination of alveolar P0 2 /arterial P0 2 gradient provides an index to the degree of pulmonary ventilationperfusion abnormalities. 5. Measuring the vital capacity, besides being difficult, is not always accurate. Usually, the results represent the least that the patient can do and under these circumstances, a reduction of 60 to 70 per cent from the patient's approximate normal would indicate ventilatory need. On the other hand, the maximum mid-expiratory flow rate is a sensitive indicator of expiratory air flow obstruction, possibly more sensitive than the one-second forced expiratory volume deterInination, and is normally 2 to 10 liters per second. A 1 to 2liters per second value may be the only abnormality seen in an otherwise asymptomatic patient, but such a level is indicative of impending respiratory failure. This test is also very helpful in measuring bronchodilator response.
Constant skilled observation is an obvious requirement, and a skilled observer will not require a laboratory to know that a patient is in distress. It is difficult, however, to judge respiratory function and ventilatory need when the patient is unconscious, in shock, and acyanotic. Signs of respiratory insufficiency in the immediate postoperative patient are minimal and can be completely obscured by oversedation or residual anesthesia. Tachypnea and tachycardia may be indicative of other problems, and in such instances laboratory findings must be utilized. Determinations of arterial pH, Pc02 , standard and actual bicarbonate, total CO 2 , base excess, P02 , and oxygen saturation of hemoglobin, as well as alveolar Pc02 and P0 2 , must be readily available on a 24-hour basis.
AIRWAY MANAGEMENT Maintaining an airway is one of the most important aspects of the care of the patient with respiratory difficulty, and must be given the utmost priority. Often, proper airway management can spell the difference between success and failure, and any delay in implementation of the necessary procedures can result in untoward complications, not least of which is loss of life. Once the existence of airway obstruction, partial or complete, has been established, an immediate hyperextension of the head and flexion of the neck may clear hypopharangeal obstruction caused by relaxation of the base of the tongue. Positive pressure inflation attempts should next be made in order to establish the effectivenesss of this maneuver, as well as to establish initial gas exchange. Clearing of the oropharynx will be necessary to prevent further obstruction and aspiration of foreign material. Forward displacement of the mandible is indicated to further eliminate physiological obstruction, and insertion of an oropharyngeal airway may be necessary. If these procedures are not successful in establishing a patent airway, or if the recovery of normal physiologic airway patency is not expected immediately, endotracheal intubation must be done. Using nasotracheal suction and an oropharyngeal airway for more than a short period of time carries potential hazards. Endotracheal intubation should therefore be considered from the outset in patients in whom manage-
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ment of secretions, the inability to insure a patent airway, or the possible need for mechanical ventilation exists. Eventual tracheostomy must be considered to insure the patency of the airway in patients in whom respiratory failure and a pending respiratory crisis coexist with difficulty in the management of secretions. Tracheostomy should never be considered an emergency procedure but rather an elective, supportive measure. According to different authors, an endotracheal tube may be left in from a few days to 2 to 3 weeks, and this adequately supports the concept of intubation before, and often instead of, tracheostomy. Access to the lower part of the airway for the purpose of removing secretions can be achieved with endotracheal tube and tracheostomy alike, technique being the major difference. Problems with endotracheal tube cuffs, often used to justify tracheostomy, are not unique, for tracheostomy tubes can create similar difficulties. Table 2 lists advantages and disadvantages of nasotracheal intubation and tracheostomy. A clinical evaluation of the individual patient will be more valuable than any discussion in determining which procedure to use.
Endotracheal Tube Once the patient has been intubated, it is necessary to confirm the position of the tracheal tube, initially through the use of a stethoscope, and later by roentgenographic examination. The tube must then be
Table 2. Advantages and Disadvantages of Nasal Endotracheal Intubation and Tracheostomy NASAL ENDOTRACHEAL TUBE
TRACHEOSTOMY
EITHER
Advantages Less interference with swallowing Easier and safer for prolonged use Easier to suction airway
Improves removal of secretions Facilitates connection of airway to respirators Reduces dead space
Esophageal compression
Infection of site
Swallowing is difficult
Bacterial contamination of airway Bleeding from trachea, carotid artery, or jugular vein Mediastinal emphysema
Obstruction of tube if inflated cuff slips Humidification and warming lost Bronchorrhea
Less interruption of body defenses Easily inserted and removed
Disadvantages
Speech is impossible May occlude one major bronchus Vocal cord damage
Harder to repeat
Kinking of tube
Extubation may be difficult
Subglottic edema
Narrow tube may not permit complete expiration so that venous return is impeded Tracheal necrosis from tube or inflated cuff Subsequent tracheal granuloma or stenosis
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secured in place with proper surgical adhesive tape, so that movement of the patient or of equipment attached to the tube does not dislodge it and cause its further movement into the right mainstem bronchus. If supportive oxygen therapy is considered at the onset, rather than mechanical ventilation, the oxygen cannula should never be placed directly into the endotracheal tube lumen. Such a catheter would reduce the size of the lumen and cause an increase in the resistance to exhalation, which is equivalent to an increase in the patient's work of breathing. Resistance to flow varies as the fourth power of the radius of a tube, so that even a slight decrease in the lumen will cause a great increase in resistance. Instead, a T-shaped adaptor may be constructed, or one of the many on the market may be used, to connect the oxygen cannula. An oxygen reservoir to increase concentration can be added to this type of adaptor, as well as increased dead space in the exhalation phase. Endotracheal suction must then be instituted immediately, as the patient no longer has the ability to cough. Large, low-pressure tracheal tube cuffs are indicated instead of small, narrow, high-pressure cuffs when artificial ventilation is required. The narrow cuff tends to increase the pressure on the tracheal wall over a small area, whereas the large, low-pressure cuff distributes a lower pressure over a wider area and tends to cause less trauma to the tracheal wall initially. However, tracheal trauma is still possible with the use of any cuff. Orotracheal Versus Nasotracheal Tubes An orotracheal tube may be used for 2 or 3 days, at which time the patient should be changed to a nasotracheal tube before the orotracheal tube can cause glottic trauma. A nasotracheal tube is easier to secure, can be tolerated well by the conscious patient, and can be used for 2 to 4 weeks, with proper supportive care. The nasotracheal tube does not irritate the tracheal mucosa as seriously as the orotracheal tube does. A major disadvantage of the nasotracheal tube is the limitation of its size by the size of the nasal opening. Tracheostomy Care The following are necessary at the bedside: Professionals trained in the care and management of the airway: a respiratory therapist or a nurse trained in airway management or both. Suction apparatus capable of achieving a vacuum equal to 120 mm. Hg. Sterile suction setup. Sterile tracheostomy dilators, or sterile Kelly clamp. Two spare tracheostomy tubes, one of the same size and one of the next smaller size, taped onto the wall above the patient's head. Humidification apparatus capable of producing 100 per cent water vapor saturation at body temperature. Endotracheal tube tray, complete and ready for use if the tracheostomy tube becomes dislodged. Good lighting. Complete, manual, self-inflating resuscitation bag, including mask and all adaptors necessary for endotracheal as well as tracheostomy tubes. A means of assessing ventilation. Pencil and paper for the conscious patient to use in communication.
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Complications of Tracheostomy The rewards of immediate or early tracheostomy are obvious, but they certainly must be weighed against the possibilities of complications. There is no ideal tracheostomy tube, and the associated complications can run the gamut from too great a delay in consideration to total obstruction of the tube, leading to asphyxiation. Each complication, therefore, is related to a specific course of action. Because of the limitation of space, these complications will only be listed.
Death. Pneumothorax, if the pleural spaces are entered. Cuff dislodgement, if the cuff on the tracheal tube slides down the barrel of the tube and occludes the distal orifice. Tracheal hemorrhage. Over-inflation of the cuff may compress the lumen of a soft tracheostomy tube. Tracheal erosion. Tracheopleural fistula. Tracheal stenosis. Tracheal dilatation. Dysphagia. Aspiration can occur in the presence of an uncuffed tracheostomy tube. Erosion of the innominate artery posteriorly. Tracheomalacia. Atelectasis may be caused by improper placement of the distal tip of the tracheostomy tube, into a major bronchus (usually the right bronchus). Improper suctioning leads to hypoxia, arrhythmia, and infection. U se sterile procedures at all times! Ineffective cuff pressure. The pressure within the balloon should not be allowed to exceed the capillary pressure. A stopcock and a manometer may be used to monitor the pressure within the tracheostomy balloon. Proper cuff inflation can be insured by inflating the cuff until a seal exists, and then backing off until there is a small leak of air audible through a stethoscope placed just superior to the tracheostomy wound. Pneumothorax related to positive pressure ventilation is overrated. It requires 80 cm. of pressure to rupture a lung out of the thorax, and considerably more when a lung is restricted by the thorax. Children are an exception. Infection secondary to respiratory therapy apparatus. Oxygen toxicity. Monitor oxygen content and titrate supplemental oxygen against increases in arterial P02 values. It is not considered necessary to maintain arterial oxygen partial pressure above 100 mm. Hg. Cardiac arrhythmia. 77 per cent of patients on ventilators have transient cardiac arrhythmias with a consequent increased mortality. These may be due to acidosis, hypoxia, electrolyte imbalance, or cardiotonic drugs. Inability to wean the patient from the ventilator. Apnea. Subcutaneous emphysema or mediastinal emphysema. Tension pneumothorax. Air embolism. Dislodging of tube. Wound infection, essentially a nursing problem reduced by education in proper techniques and precautions. Tracheal ulceration. Tracheitis. Blockage of endotracheal tube. Laryngotracheal bronchitis.
Standard Tracheostomy Care Doctors must complete and sign a standard order sheet for tracheostomy care or else must write detailed instructions. Where there is any doubt, or unless otherwise specified, nurses and respiratory therapists will follow standard procedures.
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Humidification is required on all tracheostomy patients. Patients who require more care than the usual irrigation and aspiration should be placed in the respiratory intensive care unit (e.g., those requiring ventilatory assistance). Nurses or respiratory therapists may remove the inner cannula of a metal tube for cleaning, but only physicians may change the outer cannula of a metal tracheostomy tube. The obturator, in a sterile pack, must be taped to the head of the bed, or on the chest wall. If the outer cannula is unexpectedly expelled, a nurse will remain with the patient and attempt to ventilate the patient through his nose and mouth, or through the tracheostomy opening. An aide is to summon medical aid. When a patient is on continuous ventilation, the cuff of the tube is to be deflated by the respiratory therapist (1) every hour for 5 minutes, with provisions made to compensate for the air leak; suctioning must accompany all deflation procedures; and (2) if the patient has difficulty in swallowing during meals. If a patient is to be discharged from the hospital with a tracheostomy tube in place, the teaching of the patient (and his family) should begin as soon as his condition warrants before his discharge. Decannulation must be specifically ordered in detail by the physician.
OXYGEN THERAPY With rare exceptions, oxygen should never be denied to a patient who exhibits the need for it on the basis of arterial blood gas analysis, nor should it ever be administered indiscriminately or without proper monitoring. The use of oxygen in the cardiopulmonary or respiratory emergency without due regard for the fractional inspired concentration of oxygen (F10 2 ) is considered acceptable. However, for routine therapy, or once the patient has been stabilized, a great deal of consideration must be given to maintaining the arterial P0 2 around the desired level of 100 mm. Hg. An important consideration in the administration of supplemental oxygen to a patient in acute respiratory failure is the relegation of his breathing stimulus to the peripheral chemoreceptors by a low arterial oxygen tension. Serious depression of ventilation can ensue when the patient influenced by this hypoxic drive is presented with an F 1 0 2 sufficient to reduce the stimulus to breathe. In this type of patient, an increase in the F 1 0 2 by 4 to 6 per cent will generally double the oxygen supply to the tissue. It will limit the rise of Pco 2 and avoid narcosis, ineffective cough, shallow breathing, and deterioration of the lung function. According to Campbell, small increments of inspired oxygen flows, 1 to 4liters per minute (24 to 32 per cent) have proved sufficient in obstructive lung disease, and efforts should be made to avoid higher concentrations. More ambitious methods, such as intermittent positive pressure breathing, may reduce cardiac output, reduce Pco 2 (or H+), and cause cerebral vasoconstriction, a shift of the oxygen dissociation curve to the left, and reduce the cerebral oxygen supply, even if the arterial P0 2 and saturation are normal. Any sudden fall in P0 2 under these circumstances is particularly disastrous.
Humidification Humidification of the oxygen, or any inspired gas, is absolutely mandatory, regardless of the form of delivery. Optimally, air reaching
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the carina should be at 100 per cent relative humidity at body temperature, especially in the case of tracheostomy or endotracheal intubation. Bubble-type humidifiers force a stream of oxygen through a layer of water to add water vapor to the dry gas by evaporation. A shortcoming of this type of humidifier is that water at room temperature is cooled by the evaporation process and therefore lowers the temperature of the gas that passes through it. Cooling decreases the moisture carrying capacity of the gas to allow only about 40 per cent relative humidity. Bubble-type humidifiers are used with small-bore tubing and are employed only for short-term, emergency therapy. They are absolutely inadequate to treat patients with tracheostomies or endotracheal tubes, although they may be used when the patient is receiving oxygen through a cannula or mask and thereby utilizing physiologic humidification mechanisms. Nebulizers use a gas stream, or electronic energy, to break a liquid into small particles, delivering water in droplet form as well as vapor. These droplets form a mist which represents gas supersaturated with water. Heating the water within the nebulizer chamber to well above body temperature, to allow for cooling during its delivery to the patient, usually will result in a relative humidity of 100 per cent at body temperature. Oxygen that is humidified by a nebulizer must be administered through a large-bore connecting tube, as the "rain-out" in a smaller tube, due to cooling, would soon obstruct it. Although heated humidifiers are generally indicated for the patient with a tracheostomy, it is well to withhold heat for the first 12 hours in order not to aggravate local bleeding at the site of the wound.
Hazards of Humidification Cold mist may increase metabolic demands by causing shivering. A heated nebulizer may interfere with heat loss and lead to elevated temperature, increased oxygen consumption, and eventually, an inTable 3. Complications of Therapy for Respiratory Failure Shock (50 per cent or more) Circulatory Septicemic Hypoxia and bradypnea Depression of ventilation Administration of oxygen Administration of narcotics and sedatives Extreme CO2 retention without O2 administration Ventilatory dysfunction Errors of airway management Infections (pulmonary) Oxygen toxicity Wet lung syndrome Gastrointestinal bleeding (10 to 15 per cent) and gastric dilatation Pulmonary embolism (5 to 10 per cent) Pulmonary-renal syndromes Acid-base or metabolic disturbances Arrhythmias Acute pancreatitis
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creased cardiac workload. Positive water balance and increased absorption may lead to overhydration and increased cardiac workload. Finally, humidification can be a potential source of infection - prolonged ultrasonic nebulizer therapy with normal saline may cause bronchopneumonia, loss of surfactant, atelectasis, protein exudate, and cell fragmentation of the epithelium.
Oxygen Toxicity No patient should receive more than 40 per cent oxygen, unless the arterial oxygen tension is less than 60 mm. Hg. Although no patient with hypoxia should ever be denied oxygen, its administration should be accurately and frequently monitored. The Bird "Mark 7," which is described as a "pressure generator" ventilator, is powered by compressed oxygen. The air mix control allows a mixture of gases to take place. However, the concentration of oxygen administered depends on the patient's ventilatory compliance and on the resistance to flow created by the tubing. At high pressure settings, the mechanism may malfunction, and high concentrations of oxygen may be delivered to the patient. Even with the Bird parallel inspiratory flow-mixing cartridges, the actual oxygen concentration delivered often cannot be determined by the settings alone. The higher the FIO z, the greater the toxic effects of oxygen that can be seen. Toxic effects are related to the loss of the lung's normal surface tension. Unfortunately, the pathophysiology develops long before the clinical picture when high oxygen concentrations are used. Decreasing arterial oxygen tension, necessitating an increased inspiratory oxygen concentration, should make one immediately suspect oxygen toxicity. A chest radiograph shows collapse and consolidation of the lungs. There is also an increase in ventilatory pressure with a dissociated decrease in minute ventilation Cif a volume-regulated respirator is used). Diffuse rales can be heard upon auscultation. To prevent oxygen toxicity, high concentrations of oxygen should not be administered for more than 24 to 36 hours. Arterial oxygen tension and the percentage of inspired oxygen should be monitored to maintain an arterial oxygen tension of 70 to 80 mm. Hg, or possibly 100 mm. Hg if a patient's cardiac output is good. However, if the alveolar arterial oxygen tension gradient exceeds 500 mm. Hg, continuous positive pressure ventilation should be considered. Caution must be used in the severely emphysematous patient and extreme lung volumes must be avoided. Oxygen toxicity is related to the loss of elasticity of the lungs. When the chest is opened in such a patient, no collapse of the lung is evident. The first phase is the hemorrhagic exudative stage where surfactant activity is impaired. The lungs become beefy and edematous. There are hyaline deposits, thickening of the alveolar walls, clear fluid material associated with pulmonary edema, destruction of the bronchioles, and emphysematous changes., The patient's behavior in such a manner imitates chronic obstructive lung disease, and he needs higher ventilatory pressures. The next phase is the proliferative phase a cellular fibrotic state. Increase of normal alveolar fibroblastic proliferation, a tufting of the
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capillary bed, outpouching of the alveolus, cellular proliferation, and eventually a stiff lung are the characteristics. Both phases can exist concurrently. There is a small elevation in the P aC02, which is normally harmless but has been known to aggravate the toxic effects of oxygen. Oxygen toxicity will also produce an x-ray picture of a decrease in compliance, associated with minimal aspiratable secretions and an eventual deterioration of blood gas values. There are no contraindications for oxygen therapy, but rather specific indications as governed by precautions.
INDICATIONS FOR VENTILATION The most common indication for controlled ventilation is respiratory insufficiency. Assisted ventilation may be used for any condition in which respiratory activity is either completely absent or, if present, is insufficient to maintain either adequate oxygenation or carbon dioxide clearance. It has been suggested that acute respiratory failure is present and deserving of intensive therapy if there is clinical evidence for it supported by findings of an arterial blood pH less than 7.25, arterial blood carbon dioxide tension greater than 55 mm. Hg, or an arterial blood oxygen tension less than 60 mm. Hg. Such data are more significant if they represent an acute change. Patients in respiratory insufficiency (an acutely elevated P aC02 without pH changes, with or without hypoxemia) or who are in impending respiratory insufficiency (e.g., a chronic asthmatic) should be considered candidates for ventilatory therapy too. Generally, the more rapid the deterioration and the healthier the patient before the exacerbation of the acute illness, the more likely it is that the patient will require assisted ventilation. Arterial pH and blood gas levels are useful guidelines to indicate the need for mechanical ventilation, provided that they are not used as absolutes to initiate action. Some patients with chronic pulmonary disease have a P aC02 above 50 mm. Hg but are not in respiratory failure. Patients with chronic metabolic acidosis have a low P aC02 and would be considered to be in respiratory failure if the Pco 2 were elevated. Pneumothorax without chest tubes, hemorrhagic shock, inadequate functioning of lung tissue, and unskilled personnel may be contraindications to mechanical ventilation. The Use of Ventilators In considering the mode of operation of any ventilator, it is necessary to distinguish four functions. The ventilator must inflate the patient's lungs, deflate the lungs (or allow passive expiration), have some means to "decide" when to stop inflation and start expiration, and some other means by which it "decides" when to stop expiration and start inflation again (Asmundsson). The ventilator should include at least the following characteristics: Capability of operating for long periods with a minimum of servicing and a maximum freedom from the risk of mechanical breakdown.
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Provisions for operating the instrument on room air, pure oxygen, a variable mixture of both, and any other gas desired. Dependable control over the generated pressure, whether the ventilator is pressure generated or volume generated. Variable flow control, either manual or automatic. Control of frequency. A combination of both control and assistive capabilities for greater versatility in handling the changing patterns of breathing. Negative pressure during exhalation for the patient undergoing prolonged controlled ventilation. Provisions for adequate humidification of inspired air. A means of adjusting the inspiratory-to-expiratory time ratio, or at best a provision to insure that inspiration does not exceed expiration. Some means to monitor delivered tidal volume and airway pressure. A sigh mechanism.
MONITORING Once the medical team, through the use of a mechanical ventilator, assumes a life-support function for the patient, adequate means must be established to judge the continuing effectiveness of this therapy. It is no longer enough to assess the patient's ventilatory needs by clinical observation of signs and symptoms alone. Nor is it desirable to interpret physiologic data such as that determined by blood gas analysis without consideration of a well documented clinical picture. Technological progress in the development of electronic and mechanical monitoring devices has allowed the assessment of many physiological parameters and mechanical functions. The best approach to evaluation of respiratory therapy combines the use of such devices with careful clinical observation by well-trained personnel. Even with the best care and monitoring, therapy for respiratory failure is plagued with complications (Table 3).
Clinical Monitoring Close clinical observation of the patient being maintained on mechanical ventilation is mandatory. The interpretation of signs and symptoms, based on an understanding of the physiology of the disease states responsible for the aberration of ventilatory function, can often spell the difference between averting a problem and having to treat its result. Routine auscultation of the chest is a valuable means of assessing airway patency as well as ventilatory distribution. Proper placement of an endotracheal or tracheostomy tube must also be confirmed by auscultation. The need for suctioning can be ascertained well in advance of associated compliance changes. Observation of the patient's diaphragmatic excursion and changes in the use of accessory muscles of breathing can signal an inefficiency of effort, or an increase in the work of breathing. Paradoxical movements of the epigastrium as well as distention of the abdomen may signal early complications of therapy. Cyanosis, although not a reliable sign of hypoxia, may give notice of an acute ventilation perfusion abnormality. Changes in peripheral
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circulation will also be associated with notable changes in the color of the skin. To assure adequate ventilation in certain disease states, it may also become necessary to alter the inspiratory/expiratory ratio to a point where an increase in the mean intrathoracic pressure eventually results in decreased cardiac output. Although this condition is generallyassociated with inspiratory/expiratory ratios below 1: 1, it is a consideration in any patient in whom positive pressure respiration is employed on a continuous basis. Physiologic (Analytical) Monitoring Physiologic or analytical monitoring should serve not as an alternative to continual clinical evaluation, but rather as an adjunct. An arterial blood sample should be drawn as close to the onset of the ventilatory crisis as possible - preferably prior to the institution of mechanical ventilation. This is often impossible, however, and should be deferred in situations where prompt treatment is necessary. Arterial blood gas determinations should be made within the first 10 to 15 minutes following start of mechanical ventilation. Adjustments can then be made in oxygen concentration, respiratory frequency, and tidal volume, in order to approximate the desired blood gas and acid base status. Repeated blood gas analysis every half hour (or more frequently) may well be necessary until the patient's clinical and physiologic status become stable. A patient's acid-base status may be returned to normal, generally at a rate which does not exceed that rate at which the abnormality manifested itself. A general rule of thumb concerning the return of partial pressure of carbon dioxide when accompanied by a pH change is that the P a co 2 may be lowered at a rate of approximately 10 mm. Hg per hour. This is relative and is open for interpretation on an individual basis. Great care must be taken when compensatory pH changes exist in the face of elevated carbon dioxide levels. Overzealous ventilation of this type of patient can often result in an overwhelming alkalosis. The partial pressure of arterial oxygen should be maintained within the 80 to 100 mm. Hg range. One of the drawbacks of arterial blood gas analysis has been the unavailability of attending physicians or house staff members for drawing the arterial sample. Although the decision for blood gas analysis must originate with the physician, the actual drawing of the sample can certainly be relegated to the trained respiratory therapist, a practice which has received wide attention of late. In order to stabilize the patient during the acute period, repetitive arterial sampling is usually necessary, and utilization of an indwelling arterial cannula may be considered. The insertion of an indwelling arterial catheter is a technique which should be reserved for the physician. Once a "physiological equilibrium" exists between the patient and the mechanical ventilator, and the patient can be considered stable, blood gas analysis need only be done 2 or 3 times each day. Standing orders for arterial blood gas analysis, indicating frequency, are essential. This allows the respiratory therapist or nurse to report not only the clinical situation but also the resultant physiological changes.
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In the patient in whom repeated arterial blood gas analysis is necessary, the use of the arterialized capillary sampling technique may provide an alternative. A micro sample of approximately 50 to 150 micro liters of blood is obtained from the selected site (usually the heel of the hand) after "arterializing" the area through the use of wet heat. The sample is analyzed using routine blood gas analysis techniques. Within normal physiological ranges, this technique closely approximates arterial blood gas analysis. Inaccuracies, however, are associated with the higher physiological ranges. Proper technique is essential for reliable results. The use of venous blood as an assessment of ventilatory status is not accurate, as venous blood is generally considered to reflect the tissue status of that area served by the vein selected for sample. The use of central venous blood and its correlation to arterial blood for Pc02 and pH de terminations has been discussed in recent years. In view of the difficulty in assessing the exact placement of a central venous catheter and the inability to correlate oxygen tension, it is the opinion of the authors that this method is not a reasonable alternative to arterial blood gas determination. The rebreathing technique for determining alveolar Pco2 has been shown to have direct correlation with arterial Pco2 • This method is useful for evaluating the effectiveness of alveolar ventilation, particularly when monitoring the patient in the non-acute phase. Other Monitoring Techniques Advances in technology have placed additional techniques and valuable information at the disposal of the management team. Electrocardiographic monitoring should be employed for those patients receiving augmented ventilatory support. Blood pressure, intravenous infusion rate, and respiratory rate can also be monitored electronically. Indwelling arterial blood gas electrodes make possible the continuous surveillance of blood gas status, although their use is still limited and in need of more clinical evaluation. The use of indwelling electrodes combined with expiratory gas sampling, and information gained through the use of expiratory pneumotachographic information, have made possible a continuous on-line computerized analysis of a patient's ventilatory status. Monitoring Equipment Function One of the most important considerations in assuring the success of assisted mechanical ventilation is constant surveillance of the ventilator's function, as well as the manner in which the technical aspects of ventilation are managed. All too often, situations such as "plumbing accidents," mechanical disconnections, or even failure of the management team to interpret properly the patient's status can compromise the patient's status beyond our ability to assist him. A mechanical ventilator which is being used to duplicate the mechanical and physiologic function of breathing, in addition to being in c~nstant attendance by a knowledgeable technician, should be equipped with a device that will signal disconnection. An audiovisual alarm system is the most appropriate method.
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The exhaled tidal volume should be able to be observed breath by breath. With the appearance of electronic equipment for this function, the use of positive displacement spirometers has waned; yet a great deal of information can be gained through the use of these devices. For example, slowed expiratory flow rates are easily visible on a positive displacement spirometer, whereas they may not be immediately visible through an electronic device. A mechanism to establish effectively the inspired oxygen content must also be present, and an audiovisual alarm may also be an asset. A manometer which enables the operator to determine the delivery pressure of the system is important in the monitoring scope of a ventilator. Also helpful are means whereby the inspiratory/expiratory ratio can be obtained, as well as a method to approximate compliance. This can be accomplished through tidal volume and pressure monitors. To assist in monitoring both the management and the technical aspects of ventilatory assistance, we have designed three basic flow sheets. The first is placed on the ventilator and is used for recording the initial settings of the ventilator. This sheet is kept on the ventilator, and subsequent changes placed on the sheet alert all personnel of authorized changes in settings. The second flow sheet, the "Sequential Blood Gas Data Record," is placed on the patient's chart. All blood gas data, in chronological order, are logged on this record, along with therapeutic measures which may cause subsequent alterations. This record, of course, correlates directly with the first flow sheet, in that it provides justification for changes in settings. The third sheet is a respiratory care record on which the respiratory therapist or nurse records all data relative to the ventilatory status of the patient. Medicolegal considerations make the recording and retrieval of this type of data important.
REFERENCES Amberson, J. B.: The management of acute respiratory failure in chronic bronchitis and emphysema. Amer. Rev. Resp. Dis., 96:626,1967. American Thoracic Society, Committee on Therapy: Therapy of acute respiratory failure. Amer. Rev. Resp. Dis., 93:3, 1966. Asmundsson, T., et a!.: Complications of acute respiratory failure. Ann. Intern. Med., 70: 484,1969. Bates, D. V., Macklem, P. T. and Christie, R. v.: Respiratory Function in Disease. 2nd ed. Philadelphia, W. B. Saunders Company, 1971. Belinkoff, S.: Introduction to Inhalation Therapy. Boston, Little, Brown & Co., 1969. Bendixon, H. H.: Respiratory Care. St. Louis, C. V. Mosby Co., 1965. Birley, D. M., et al.: The place of the intensive therapy unit in the general hospital. Acta Anaesth. Scandinav., vol. 23, suppl. 92, 1966. Campbell, D.: Four years of respiratory intensive care. Brit. Med. J., 4:255,1969. Comroe, J. H., et a!.: The Lung. 2nd ed. Chicago, Yearbook Medical Publishers, 1962. Dines, D. E., et al.: Monitoring certain aspects of respiratory failure. Dis. Chest, 54:421, 1968. Egan, D. C.: Fundamentals of Inhalation Therapy. St. Louis, C. V. Mosby Co., 1969. Feldman, S. A.: Tracheostomy and Artificial Ventilation. Baltimore, Williams & Wilkins, 1967. Handbook of Physiology, Section III (Respiration), vols. 1 and 2. Washington, American Physiological Society, 1964-1965. Hayman, L. D.: Policies and procedures of an intensive care unit. North Carolina Med. J.. 1968, p. 250. Kibelstis, J. A.: Management of respiratory failure. AFP/GP, 2:90,1970. Mushin, W. W., et al.: Automatic Ventilation of the Lung. 2nd ed. Oxford, Blackwell Scientific Publishers, 1969. Noehren, T. H., et al.: The ventilation unit for special intensive care of·patients with respiratory failure. J.A.M.A., 203:641, 1968.
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O'Donohue, W. J., Jr., et al.: The management of acute respiratory failure in an RICU. Chest, 56:603, 1970. Petty, T. L.: P.S. Don't forget the respiratory intensive care unit. Dis. Chest, 56:276, 1969. Petty, T. L., et al.: Management of acute respiratory failure (a systemic approach). Ann. Allergy, 26:405, 1968. Petty, T. L., et al.: The intensive respiratory care unit. California Med., 107:381, 1967. Petty, T. L., et al.: Comprehensive care program for airway obstruction. Ann. Intern. Med., 70:1109,1969. Ramachandran, P. R., et al.: Changes in functional residual capacity during respiratory failure. Canad. Anaesth. Soc. J., 17:359, 1970. Rogers, R. M.: Respiratory insufficiency: Treatment with mechanical ventilators. Medical Times, 98:197,1970. Safar, P.: Respiratory Therapy. Philadelphia, F. A. Davis Co., 1965. Segal, M. S.: Treatment of acute respiratory failure. New Eng. J. Med., 274:841,1966. Shelley, M. K.: Acid-base measurements in intensive care. Biomed. Sci. Instrum., 5:41, 1969. Stone, D. T.: Management of ventilation failure. New York State J. Med., 1970. Sykes, M. K.: Accessories for humidifiers. Anaesthesia, 22:668, 1967. Tse, R. L., and Lee, M. W.: pH of infusion fluids. J.A.M.A., 215:642,1971. Tysinger, D. S.: The place of respiration in the coronary care unit. J. Med. Assoc. State of Alabama, 39:355, 1969. Wagner, W. W., Jr., et al.: Pulmonary gas transport time: Larynx to alveolus. Science, 163: 1210, 1969. Warrell, D. A., et al.: Effects of controlled oxygen therapy on arterial blood gases in acute respiratory failure. Brit. Med. J., 2:452, 1970. Whipple, H. E., ed.: Respiratory failure. Ann. N.Y. Acad. Sci., 121 :651, 1965. Winter, P. M., et al.: Acute respiratory failure. Scientific American, 221 :23,1969. Valley Hospital Ridgewood, New Jersey 07450