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Phrenic nerve pacing--an alternative to positive pressure ventilation: the required nursing care.

Phrenic nerve pacing as a method of ventilation was first recognized in 1783. For years, this technique was not used because of the lack of practical technology. Interest in phrenic nerve pacing was renewed in the 1960s with the development of a radio frequency transmission system. Applicable to a limited patient population, phrenic nerve pacing has several benefits over positive-pressure ventilation. Benefits include greater patient mobility, verbal articulation, less mechanical noise, and breathing by natural negative-pressure. This article provides information for nurses who care for patients ventilated by phrenic nerve pacing.

Diaphragm↗

Historical perspectives on the development and use of mechanical ventilation.

Contemporary advancements in cardiothoracic and abdominal surgical procedures have been historically dependent on the development and adoption of controlled airway management, specifically endotracheal intubation, controlled positive-pressure ventilation, and the use of automatic positive-pressure mechanical ventilators. More than 400 years elapsed before the 16th Century theories of Paracelsus and the demonstrations of Vesalius were routinely adopted to solve the "pneumothorax problem" that prevented complicated or prolonged surgical procedures within the pleural cavity. Acceptance and implementation of controlled positive-pressure ventilation was impeded for decades by the inability to maintain and protect the airway. Consequently, emphasis on the development of mechanical ventilation was directed toward machinery that provided safer negative-pressure respiratory support. The introduction of curare into European anesthesia practice and the adoption of protective airway practices during the poliomyelitis epidemics led to routine use of controlled positive-pressure ventilation and construction of dependable machinery. Laboratory investigations, exploring complications from cardiothoracic surgery, brought about American acceptance and established controlled positive-pressure mechanical ventilation as an indispensable part of conventional intraoperative management.

Europe↗

A comparison of two different bronchial cuff designs and four different bronchial cuff inflation methods.

OBJECTIVE: To compare directly measured pressures at the cuff/trachea interface that are associated with two different bronchial cuff designs and four different methods of bronchial cuff inflation suggested for use with one-lung ventilation. DESIGN: In vitro study. SETTING: Experimental laboratory in a university-affiliated hospital. INTERVENTIONS: The bronchial cuffs of two different endotracheal tubes were inflated using one of four different methods of determining the cuff volume and pressure necessary to "just seal" the bronchus and obtain lung separation; positive-pressure test, negative-pressure test, CO2 analysis, and a new test using an anesthesia ventilator. When each method predicted the "just-seal" state, the pressure at the cuff/bronchus interface as well as cuff inflation pressure and volume were recorded. MEASUREMENTS AND MAIN RESULTS: Although the new test was incompatible with the bronchial blocker, the other three tests all accurately predicted lung separation with the Univent, with no significant differences in pressures exerted on the trachea. However, when used with the double-lumen tube, the new test produced significantly lower measured parameters than the other inflation methods. CO2 analysis did not reliably predict bronchial seal with the double-lumen tube. CONCLUSIONS: To achieve lung separation with the lowest pressure on the trachea, the new test is the most appropriate method for use with the double-lumen tube; however, the negative-pressure test appeared to be the easiest and fastest method for use with the bronchial blocker. Although the bronchial blocker was associated with lower pressures transmitted from the cuff to the trachea, the in vitro model cannot predict which bronchial cuff design would be superior in vivo.

Adult↗

Negative-pressure pulmonary edema in the otolaryngology patient.

It is estimated that 11% of all patients requiring active intervention for acute upper airway obstruction develop negative-pressure pulmonary edema. This pathologic process typically has a benign and rapidly resolving clinical course with the prompt use of mechanical ventilation and positive end expiratory pressure. A review of the literature, however, has revealed a morbidity and mortality rate of 11% to 40% in reported series. During the years 1991 through 1993, six patients were identified in whom negative-pressure pulmonary edema developed after various otolaryngologic procedures. Five (84%) of the six patients had complete resolution of the pulmonary edema within 24 hours, and the sixth patient progressed to prolonged mechanical ventilation and eventual death. In an effort to further understand the pathophysiology of this disease, a cardiac evaluation was performed by use of echocardiography on all six patients. In three of the six patients, studies revealed an underlying cardiac anomaly not previously identified by history or physical examination. Findings included one case of hypertrophic cardiomyopathy and two cases of pulmonary and tricuspid valvular insufficiency. This 50% incidence of cardiac anomalies is striking, in contrast to the less than 1% incidence of these anomalies in the general adult population. To our knowledge, this is the first study to implicate an underlying cardiac cause for the generation of negative-pressure pulmonary edema. On the basis of this study, we recommend that echocardiography be a part of the routine evaluation of all patients who manifest negative-pressure pulmonary edema.

Acute Disease↗

Ventilatory responses to increased blood flow and decreased lung volume in awake dogs.

The effect of decreased lung volume on ventilatory responses to arteriovenous fistula-induced increased cardiac output was studied in four chronic awake dogs. Lung volume decreases were imposed by application of continuous negative-pressure breathing of -10 cmH2O to the trachea. The animals were surgically prepared with chronic tracheostomy, indwelling carotid artery catheter, and bilateral arteriovenous femoral shunts. Control arteriovenous blood flow was 0.5 l/min, and test flow level was 2.0 l/min. Arterial blood CO2 tension (PaCO2) was continuously monitored using an indwelling Teflon membrane mass spectrometer catheter, and inhaled CO2 was given to maintain isocapnia throughout. Increased fistula flow alone led to a mean 52% increase in cardiac output (CO), whereas mean systemic arterial blood pressure (Psa) fell 4% (P less than 0.01). Negative-pressure breathing alone raised Psa by 3% (P less than 0.005) without a significant change in CO. Expired minute ventilation (VE) increased by 27% (P less than 0.005) from control in both of these conditions separately. Combined increased flow and negative pressure led to a 50% increase in CO and 56% increase in VE (P less than 0.0025) without any significant change in Psa. Effects of decreased lung volume and increased CO appeared to be additive with respect to ventilation and to occur under conditions of constant PaCO2 and Psa. Because both decreased lung volume and increased CO occur during normal exercise, these results suggest that mechanisms other than chemical regulation may play an important role in the control of breathing and contribute new insights into the isocapnic exercise hyperpnea phenomenon.

Animals↗

Pulmonary edema following post-operative laryngospasm: a case report and review of the literature.

The pathophysiology of acute, negative-pressure pulmonary edema following post-anesthetic laryngospasm (PLPE) is unclear. We present a patient and review the literature to propose etiology and management. Nineteen reported patients (3 female, 16 male, aged 3 months to 60 years) with PLPE had undergone 10 otolaryngologic, three orthopedic, four skin/soft tissue, one intraabdominal, and one ophthalmologic procedures. Twelve patients (63%) had significant medical history. Initial intubation was performed without difficulty in 17 patients, there were no predisposing trends in anesthetic management, and post-anesthetic extubation was performed without difficulty in 18 patients. Thirteen patients developed laryngospasm in less than 2 minutes. Eight were ventilated with bag/mask, 15 required reintubation, and nine required paralysis. Onset of PLPE was less than 3 minutes in 12 patients; chest roentgenograms showed edema in 17 patients. Mechanical ventilation was required for less than 24 hours in all patients. PLPE cleared in less than 24 hours in most patients. Furosemide was administered in nine patients, digoxin in one, theophylline in two, and steroids in four patients. The precise pathophysiologic mechanism of PLPE is unclear despite numerous proposed mechanisms. PLPE resolves rapidly with short-term ventilatory support. Use of diuretics/airway dilators is variable, and their contribution to management is unclear.

Adolescent↗

Negative pressure artificial respiration: use in treatment of respiratory failure of the newborn.

Ninety-one infants with respiratory failure secondary to primary pulmonary disease and with a birth weight of 1000 g. or over have been managed in a negative-pressure respirator (Air-Shields) over a three-year period. Of these the failure in 87 was due to respiratory distress syndrome (RDS) and in four it resulted from massive meconium aspiration. Respiratory failure was indicated initially by arterial blood gas tensions (while breathing 100% O(2)) of Po(2) <40 mm. Hg, pH <7.10 and Pco(2) >75 mm. Hg in the initial 47 cases; these levels were subsequently raised to Po(2) < 50 mm. Hg, pH <7.20 and Pco(2) >70 mm. Hg for the remainder. Fifty-four (59.3%) of the infants survived the use of the respirator and 47 of these (51.6%) were subsequently discharged alive and well. Mean time in hours to normalization of blood gas values while on the respirator were as follows: for Po(2), 10.5; for pH, 11.6; and for Pco(2), 22.6. These values indicate that the respirator is more efficient in promoting oxygenation (raising Po(2)) than ventilation (lowering Pco(2)). They also suggest that the observed acidosis is in large part secondary to the hypoxia rather than the result of co(2) retention. For the survivors the average time of total respirator dependency before commencement of weaning was 53.7 hours. All the infants were managed without the use of endotracheal tubes although the use of the respirator and/or administration of 100% oxygen were either continuous or intermittent for periods of up to two weeks. There have been no instances of so-called respirator lung disease in the survivors or in those who died, which suggests that the use of high oxygen concentration by itself is not the major factor in the pathogenesis of this complication.

Age Factors↗

[Hypoventilation due to disconnection of the vaporizer and negative-pressure leak test to find disconnection].

Most of Ohmeda anesthesia machines have a outlet check valve located in the low-pressure circuit, and this influences the type of leak test greatly. We report a case of hypoventilation due to a gas leakage from the junction of two vaporizers, Fluotec 3 and Enfluratec of Ohio 30/70. This gas leakage was not discovered preoperatively by performing traditional leak test of squeezing the bag filled with oxygen. Following intubation of the trachea the patient was paralyzed and mechanically ventilated. Her vital signs were stable and operation was started. Soon thereafter, she became hypertensive in spite of increases in concentration of enflurane and supplemental doses of fentanyl and diltiazem. ETCO2 showed 7.4% and spontaneous respiration started. We checked anesthesia machine and found a gas leakage at the junction of two vaporizers. Anesthesia machine was exchanged. The remainder of the procedure was uneventful and the patient showed a normal recovery. The outlet check valve closes when back-pressure is exerted on it, and a vulnerable area including flow tubes and vaporizers is not tested by the traditional positive-pressure leak test squeezing bag. Ohmeda recommends the use of a negative pressure leak test with suction bulb device. We propose manufacturers to place a cation on anesthesia machine such as -- "Negative-pressure leak test is inevitable because of presence of outlet check valve."

Anesthesiology↗

Evaluation of new in-facepiece sampling procedures for full and half facepieces.

Precision and bias were determined on five different methods of conducting in-facepiece sampling. In-board penetration occurred through fixed, circular, leak geometries positioned at different areas on the face-seal of full and half facepiece negative-pressure respirators. The sampling procedures evaluated in the study were: (1) a continuous, low sampling rate, flush on the respirator, mid nose-mouth probing (CLF) procedure; (2) a continuous, high sampling rate, deep front-of-mouth probing (CHD) procedure; (3) a pulsed exhalation, deep front-of-mouth probing (PED) procedure; (4) an exhalation value discharge (EVD) procedure; and (5) a pulsed inhalation, deep front-of-mouth, probing (PID) procedure. The CLF procedure represents a recommended in-facepiece sampling procedure in the United States. Evaluations were done on populations of nine full facepiece respirators and five half facepieces. The full facepieces were not equipped with nose cups. The average sampling biases on the full facepieces were: (1) CLF procedure, -21%; (2) CHD procedure, -3%; (3) PED procedure, 0.7%; (4) EVD procedure, -14%; and (5) PID procedure, -12.3%. On the five half facepiece respirators the average sampling biases were: (1) CLF procedure, -26%; (2) CHD procedure, -13%; (3) PED procedure, -4%; (4) EVD procedure, -2%; and (5) PID procedure, -24%. The bias observed with each method was found to be affected, to some extent, by the location of the face-seal penetration.

Analysis of Variance↗

Negative-pressure pulmonary edema with a patent airway.

Negative pressure is a rarely occurring cause of pulmonary edema. It has previously been reported only in the presence of a closed glottis or obstructed airway. A 64-year-old man with 74% body surface burn without any inhalation injury experienced acute pulmonary edema on hospital day 11 associated with high-minute volume and negative inspiratory pressures at the ventilator. The edema cleared after sedation and paralysis. Workup disclosed pulmonary emboli and normal cardiac-filling pressures. A mechanical model, simulating his breathing, measured intrathoracic pressure of -37 +/- 12 mm Hg, which is sufficiently negative to cause pulmonary edema despite a patent airway. Pulmonary emboli increased his respiratory drive to amounts greater than what the ventilator could deliver, thus leading to the large negative intrathoracic pressure and pulmonary edema.

Burns↗

Positive- and negative-pressure breathing in newborn rat before and after anesthesia.

We have examined the effects of changes in functional residual capacity (FRC), determined by positive and negative body surface pressures, on the breathing pattern of intact newborn rats, before and after barbiturate anesthesia. With distending pressures (between 1 and 4 cmH2O) minute ventilation decreased mainly due to a prolongation of the expiratory time. This response was more marked after anesthesia and accompanied by a fall in tidal volume. The time of peak expiratory flow (TE'), an index of expiratory flow resistance, was not changed before anesthesia and only slightly decreased after anesthesia. With collapsing pressures between 1 and 2 cmH2O only small changes in breathing pattern occurred, whereas the TE' increased in all cases and the flow profile indicated a maintenance of lung volume during expiration. These data indicate that tonic vagal information is present in the newborn rat and is substantially enhanced after barbiturates. The result that changes in breathing pattern are not fully matched by the changes in TE' and expiratory flow profile may indicate that the receptors which control the respiratory pattern are not the same as those involved in the regulation of the expiratory flow. The pressure-volume curve of the respiratory system was similar before and after anesthesia, and the intercept was close to the zero pressure value, indicating that the FRC of the newborn rat, differently from the human baby, is not actively maintained above the resting volume of the system.

Anesthesia↗

Reflex effects and receptor responses to upper airway pressure and flow stimuli in developing puppies.

We studied the changes in breathing pattern due to pressure and airflow stimuli applied to isolated upper airway in nine 1- to 14-day-old and six 29- to 35-day-old anesthetized puppies breathing through a tracheostomy. Negative-pressure and flow, both inspiratory and expiratory, altered the breathing pattern only in the 1- to 14-day-old puppies, whereas positive pressure was ineffective in both age groups. Negative pressure caused apnea in 12% of the trials, expiratory flow in 18%, and inspiratory flow in 21%. When apnea did not occur there was a significant prolongation of inspiratory and expiratory time and a decrease of tidal volume of the first breath following the application of negative pressures. Section of the superior laryngeal nerves abolished the responses to pressure and flow. In nine 1- to 14-day-old and four 29- to 35-day-old puppies we recorded the activity of single units of the superior laryngeal nerves. We identified specialized receptors responding to pressure (68.5%), flow (2.7%), and contraction of upper airway muscles (drive, 28.8%). All types of receptors had a prevalent inspiratory-related activity. In the younger age group the discharge rate of pressure receptors at comparable negative pressures was lower than in older puppies. The strong inhibitory influences originating from the upper airway in the early stages of development presumably reflect different integrative properties of the central nervous system.

Animals↗

Atrial receptors and renal function.

The hypothesis that receptors in the heart or pulmonary vasculature initiate a reflex that influences urine flow was derived from experiments designed to evaluate the effect of mechanical ventilation on renal function. These experiments indicated that urine flow usually decreases during positive-pressure breathing and usually increases during negative-pressure breathing. It was surmised that impulses from certain cardiopulmonary receptors affect the secretion of ADH, which in turn influences urine flow. A subsequent investigation appeared to localize the pertinent receptors to the left atrium, but the results of this particular investigation were influenced by several complication factors that have not been widely appreciated. The apparent localization of volume-regulating recpetors to the left atrium and the accumulating evidence that atrial receptors do respond to changes in atrial pressure or atrial volume triggered a myriad of further studies on the function of left receptors. Nearly all these studies employed indirect techniques that produced changes in systemic and pulmonary hemodynamics in addition to changes in left atrial pressure. Nevertheless, it often was assumed that if changes in left pressure were produced, any concomitant changes in circulating ADH or in urine flow were attributable to a reflex elicited from atrial receptors. Mush of the data obtained were interpreted as being compatible with the elft atrial volume-receptor hypothesis, but very liggle of the data pertained to left atrial receptors specifically.

Animals↗

Maximal static pressures and lung volumes in a child with Guillain-Barré syndrome ventilated by a cuirass respirator.

Serial maximal static pressure and lung volume measurements were made in a child with Guillain-Barré syndrome and respiratory failure. The patient received successfully ventilatory support for seven weeks with the use of a cycled negative-pressure cuirass-type respirator obviating prolonged intubation and tracheostomy. The fall in VC preceded the loss of respiratory muscle strength (RMS) and lagged behind RMS in the return towards normal values. There was a disproportionate loss of lung volume (lowest VC, 220 to 250 ml, 11 to 12 percent of normal) as compared to maximal static pressures (lowest PImax, 60 cm H2O, lowest PEmax, 47 cm H2O). The disproportion was greater than that previously reported in adults. The greater loss in lung volume may be due to greater chest wall compliance in the child, resulting in less outward recoil of the chest wall and subsequently more microatelectasis with denervation of the chest wall musculature. Loss of lung volume resulted in a smaller surface area over which the respiratory muscles exerted their force. Thus, pressure being equal to force divided by surface area, could be relatively maintained and not reflect the extent of the loss of muscle force.

Child↗