Cardiovascular effects of conventional positive pressure ventilation and airway pressure release ventilation.

The hemodynamic sequelae of conventional positive pressure ventilation (CPPV), airway pressure release ventilation (APRV), and spontaneous breathing were compared with continuous positive airway pressure (CPAP) in ten anesthetized dogs who had ventilatory failure with and without parenchymal lung injury. The APRV corrected respiratory acidosis without significantly effecting arterial blood oxygenation, venous admixture, cardiovascular function, or tissue oxygen utilization. Application of CPPV precipitated marked depressions in blood pressure, stroke volume, and cardiac output. A concomitant decrease in venous admixture did not compensate for these adverse cardiovascular effects. Deterioration of tissue oxygen delivery resulted in oxygen supply-demand imbalance during CPPV. The results of this experimental study indicate that if ventilatory augmentation of subjects who require CPAP is desired, APRV will enhance alveolar ventilation without compromising circulatory function and tissue oxygen balance, whereas CPPV will impair cardiovascular function significantly.

Airway pressure release ventilation (APRV). A human trial.

After operative coronary revascularization, 14 consenting adults received conventional positive pressure ventilation (PPV). When they were hemodynamically stable, data were collected during PPV and then during airway pressure release ventilation (APRV). During APRV, airway pressure (Paw) was reduced periodically at the lowest frequency which produced normal PaCO2. As anesthesia resolved, the rate of APRV breaths was decreased until patients breathed only with CPAP. During PPV and APRV, pHa, PaO2/FIO2, and hemodynamic variables were similar. All patients were weaned from APRV without complication. Optimal ventilator design for patients with acute lung injury would provide CPAP as a primary intervention and secondarily would augment alveolar ventilation. The APRV supported oxygenation and ventilation in patients with mild acute lung injury, yet with much lower peak airway pressure than produced by PPV.

Lung mechanics and oxygen consumption during spontaneous ventilation and severe heart failure.

The effects of acute heart failure on lung mechanics and oxygen consumption (VO2) during normocarbic spontaneous ventilation were studied in 21 anesthetized pigs. Heart failure severe enough to double oxygen extraction (O2ex) was induced with intravenous esmolol boluses and infusion. Compared to normal, the inspiratory elastic work of breathing (Wel) increased from 335 +/- 371 (mean +/- SD) to 559 +/- 48 mm Hg.ml (p less than 0.003) during heart failure, lung compliance (CL) fell from 121 +/- 144 to 22 +/- 15 ml/mm Hg (p less than 0.05), and respiratory power climbed from 140 +/- 200 to 245 +/- 214 mm Hg.ml.min-1 (p less than 0.002). These mechanical changes were accompanied by a decrease in both VO2 (221 +/- 61 to 191 +/- 50 mlO2/min, p less than 0.05) and oxygen delivery (DO2) (680 +/- 240 to 260 +/- 90 mlO2/min, p less than 0.004). The VO2/DO2 ratio doubled (p less than 0.0002), confirming increased O2ex. In conclusion, severe acute heart failure decreased CL, and increased Wel and respiratory power significantly. The depressed cardiac output limits both DO2, and to some extent, VO2. However, a greater proportion of the delivered O2 is consumed, supplying indirect evidence which suggests that the respiratory muscles' VO2 increases as a consequence of increased power expenditure.

Prevention of postoperative pulmonary complications with CPAP, incentive spirometry, and conservative therapy.

Continuous positive airway pressure (CPAP) administered at intervals with a mask and incentive spirometry (IS) were compared with a regimen of coughing and deep breathing (CDB) to determine which promoted the most rapid recovery of pulmonary function after upper abdominal operations in 65 adults. Postoperatively, FRC of patients in all groups was similar relative to preoperative values. However, mean FRC of patients who received CPAP increased more rapidly than did mean FRC of those receiving CDB when compared to the values obtained following operation (p less than 0.05). Incentive spirometry did not increase FRC to a greater extent than did CDB. Roentgenographic evidence of atelectasis 72 hours postoperatively was observed in 23 percent of CPAP patients (five of 22) and 42 percent and 41 percent of patients who received CDB (eight of 19) and IS (nine of 22). Two patients (3 percent) developed pneumonia. The low incidence of pneumonia regardless of the type of therapy may be attributable to vigorous, vigilant respiratory care in a population at high risk for developing pneumonia. Frequency and supervision of respiratory therapy may be more important than the type of therapy delivered after upper abdominal operations. Mask CPAP offers advantages because it requires no effort from the patient, and therapy is not painful.

Effect of pleurotomy on pulmonary function after median sternotomy.

To determine whether pleurotomy during median sternotomy worsens postoperative pulmonary function, patients whose pleurae remained intact (N = 7) were compared with those whose pleural spaces were entered during median sternotomy (N = 31). Thirty-eight adults performed spirometry and N2 washout to determine functional residual capacity preoperatively and 2, 24, 48, and 72 hours after extubation. Two mediastinal drainage tubes were placed in every patient; no pleural drainage tubes were inserted. Chest roentgenograms were performed preoperatively and 24 and 72 hours after extubation. Preoperatively, functional residual capacity, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and FEV1/FVC did not differ between groups. Postoperatively, in all patients developed a restrictive pulmonary defect, but mean functional residual capacity, FVC, FEV1 and FEV1/FVC did not differ between groups. In contrast to earlier reports, entering the pleural space did not worsen the restrictive pulmonary defect that results from median sternotomy when direct pleural drainage was avoided.

Capnography for adults.

Capnography is the measurement of carbon dioxide (CO2) concentration in a gas mixture. This article discusses the clinical applications and limitations of capnography and end-tidal CO2 monitoring. In addition, an evaluation of the technical aspects insofar as to whether they limit or enhance clinical application and the physical principles on which the monitors' functions are based.

Noninvasive carbon dioxide monitoring.

Technical aspects and clinical applications of the two most commonly used noninvasive CO2 monitors, capnography and transcutaneous monitoring, are discussed. Neither accurately reflect PaCO2 in most critically ill patients. However, both monitors give valuable information about other aspects of the patient's physiology. PETCO2 reflects changes in pulmonary perfusion and deadspace ventilation; and, PtcCO2 reflects changes in peripheral perfusion. Thus, both are useful in the critically ill patient, but not necessarily for the assessment of PaCO2.

The PaCO2 rate of rise in anesthetized patients with airway obstruction.

Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO2 because it requires a continuous O2 flow. The CO2 rate of rise in anesthetized humans with airway obstruction was measured. Fourteen consenting healthy adults were monitored continuously with pulse oximetry and EKG. Enflurane--O2 anesthesia was established for at least 10 minutes with normal PaCO2 without neuromuscular blockade so that anesthesia was deep enough to prevent spontaneous ventilation. Then, patients' tracheal tubes were clamped. Arterial blood samples were obtained before and after 0, 20, 40, 60, 120, 180, 240, and 300 seconds after clamping, provided that oxyhemoglobin saturation exceeded 0.92. The equation that best described the PaCO2 rise was a logarithmic function. Piecewise linear approximation yielded a PaCO2 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg/minute thereafter. These values should be employed when estimating the duration of apnea from PaCO2 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant CO2 quantities.

The carbon dioxide rate of rise in awake apneic humans.

Currently available estimates of the PaCO2 rate of rise in resting humans with resting lung volume were gathered during general anesthesia. The PaCO2 rate of rise during apnea in awake subjects was determined to acquire a value that may be more applicable to awake, ventilator-dependent, critically ill patients. Clinically, apnea occurs at functional residual capacity. With FiO2 = 1.0, 20 volunteers held their breaths at functional residual capacity for 0, 10, and 20 seconds, and then for as long as possible. They exhaled through an infrared CO2 analyzer after each interval to determine end-tidal pCO2. An estimate of the logarithmic PaCO2 rise during breath holding at functional residual capacity was 7 mmHg during the first 10 seconds (43 mmHg/minute), 2 mmHg during the next 10 seconds (13 mmHg/minute), and 6 mmHg/minute thereafter. In conclusion, PaCO2 increases more rapidly in awake apneic humans than earlier thought. The values reported herein probably are better for estimating duration of apnea in conscious, critically ill patients than are values obtained during general anesthesia.

Bradycardia during cold ocular irrigation under general anaesthesia: an example of the diving reflex.

A case of bradycardia is reported which was precipitated by cold normal saline applied to the eye during general anaesthesia. The history and physiology of the diving reflex is discussed and we believe that these data suggest that this patient's bradycardia was induced by the diving reflex, and not by the oculocardiac reflex.

Oxygen consumption calculated from the Fick equation has limited utility.

OBJECTIVE: To determine if oxygen consumption (VO2) calculated using the Fick relationship (calculated VO2) determines total body VO2 accurately and precisely enough to employ this method during clinical assessment of oxygen transport. DESIGN: Methods comparison, using repeated measures during four physiologic states: normal heart/normal lungs, heart failure/normal lungs, normal heart/acute lung injury, heart failure/acute lung injury. SETTING: University research laboratory. SUBJECTS: Thirteen adult Yucatan pigs. INTERVENTIONS: Oleic acid-induced acute lung injury; heart failure was induced with a continuous infusion of esmolol. MEASUREMENTS AND MAIN RESULTS: Calculated VO2 was determined by multiplying thermodilution cardiac output by the arterialvenous oxygen content difference in anesthetized, spontaneously breathing animals. Conditions were tightly controlled so that calculated VO2 would be as accurate as possible. "True" VO2 was measured simultaneously with a water-sealed spirometer (spirometry VO2). Calculated VO2 and spirometry VO2 were determined and analyzed during the four physiologic states listed above. Pooled data also were evaluated. Mean spirometry VO2 and calculated VO2 differed significantly during all four physiologic states and when data were pooled (spirometry VO2 273 +/- 70, calculated VO2 178 +/- 58 mL/min; p < .01). Calculated VO2 consistently underestimated spirometry VO2, as demonstrated by the large, positive bias in pooled data (95 +/- 59 mL of oxygen/min) and in the four physiologic states. Linear regression of data from all four states yielded slopes that were indistinguishable from 1, but y intercepts that varied from -152 to +182. For pooled data, the following equation was used: calculated VO2 = 0.5 x (spirometry VO2 + 46); r2 = .35. Precision in pooled data was 22% of the mean spirometry VO2. Data analysis for the four physiologic states demonstrated results similar to those results obtained when data were pooled. CONCLUSIONS: Even in a tightly controlled, clinical simulation in the laboratory, calculated VO2 from the Fick relationship systematically underestimated VO2 measured with a water-sealed spirometer. If true VO2 changes, the magnitude and direction of change will be reflected by calculated VO2 but with approximately 20% error in the absolute value. Heart failure, acute lung injury, and their combination did not affect the accuracy of calculated VO2. Therefore, calculating VO2 using the Fick relationship is too inaccurate to be used for research purposes. Because assessment of the directional change of VO2 may be clinically useful, calculated VO2 can be employed with discretion during clinical oxygen transport evaluation, bearing in mind the calculation's inherent imprecision.

Intermittent mandatory ventilation (IMV): a primary ventilatory support mode.

Respiratory therapy should be directed at underlying pathophysiology, not symptomatology. Mechanical ventilation, oxygen, and CPAP should be administered to patients independently and in appropriate amounts. Removal of each of these therapeutic interventions should occur in a similar fashion. The method for determining optimal mechanical ventilation, oxygen concentration, and CPAP level is not unlike that recommended for many other therapeutic interventions. Each should be applied to achieve a predetermined goal, each should be continually reevaluated, and each should be withdrawn when indicated. Optimal CPAP should be applied to improve matching of ventilation and perfusion and to improve pulmonary mechanics so that the requirement for oxygen and mechanical ventilation is reduced. A reduction in inspired oxygen concentration may prevent absorption atelectasis and allow more rapid discontinuation of mechanical ventilation and CPAP. Minimal mechanical ventilatory support eliminates iatrogenic respiratory alkalosis and improves distribution of ventilation. This approach minimizes the detrimental effects of mechanical ventilatory support on acid-base balance and cardiovascular function and decreases the possibility of pulmonary barotrauma. Twelve years of prospective evaluation have demonstrated numerous advantages of IMV. This approach has simplified the management of patients with compromised respiratory function and has decreased morbidity and mortality (10).

Airway pressure release ventilation.

Airway pressure release ventilation (APRV) delivers continuous positive airway pressure (CPAP) and may support ventilation simultaneously. This investigation tested whether, after acute lung injury (ALI), APRV promotes alveolar ventilation and arterial oxygenation without increasing airway pressure (Paw) above the CPAP level and without depressing cardiac function. Ten anesthetized dogs randomly received either intermittent positive-pressure ventilation (IPPV) or APRV. APRV was delivered with a continuous-flow CPAP system. Expiration occurred when a switch in the expiratory limb opened and Paw decreased to near-ambient, which decreased lung volume. After baseline data collection, ALI was induced by infusing oleic acid iv. Two hours later, IPPV and APRV were administered randomly, and data were collected. With normal lungs, APRV and IPPV achieved similar gas exchange and hemodynamic function. During ALI, arterial oxygenation was improved, and peak Paw which did not exceed the CPAP level, was lower during APRV. Similar minute ventilations were delivered by both modes but resulted in lower PaCO2 with APRV. Thus, APRV decreased physiologic deadspace ventilation. Hemodynamic status was similar during both modes. Therefore, APRV is an improved method of oxygenation and ventilatory support for patients with ALI that will allow unrestricted spontaneous ventilation and may decrease the incidence of barotrauma.

Pulmonary function before and after prolonged continuous positive airway pressure by mask.

This investigation examined whether prolonged continuous positive airway pressure (CPAP) applied by face mask could sustain an increase in functional residual capacity (FRC). Before median sternotomy, nine adults performed multiple-breath nitrogen washout to determine FRC and spirometry. The day after operation, lung volumes were measured before and 10 min after the 4-h application of 7.5 cm H2O of CPAP with a mask. Mean FRC, forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and FEV1/FVC after CPAP were similar to pretreatment values. Although CPAP can restore FRC to preoperative values, and did increase FRC in these patients, FRC deteriorates within 10 min after CPAP is removed. Therefore, when a sustained increase in FRC is desired after median sternotomy, CPAP should be applied without interruption.

A linear approximation of Brody's equation to predict oxygen consumption in adult humans.

OBJECTIVE: The objective of our study was to derive a linear approximation to Brody's equation for oxygen consumption as a simpler alternative for the clinician. METHODS: The approximation was derived by using calculus to construct a line tangent to Brody's equation at 81 kg. RESULTS: The linear approximation was derived to be: VO2 = (2.5w + 67.5) ml/min, where w is the subject's weight in kilograms. The error introduced by this linear approximation is 10.9% at 30 kg and 1.35% at 120 kg. CONCLUSIONS: This linear equation may have utility for approximating oxygen consumption when an approximation is required, as in closed circuit anesthesia. The utility of this equation is that it is linear and produces a result similar to Brody's equation.

Is 50% oxygen harmful?

Pulmonary gas exchange after tracheal extubation was evaluated in 25 patients to determine the effect of 50% oxygen administered during mechanical ventilation following aortocoronary bypass grafting. Twenty-five patients received postoperative mechanical ventilation for 16 to 24 h, 13 with an inspired oxygen fraction (FIO2) of no more than 0.30 and 12 with an FIO2 of 0.50. After tracheal extubation, all patients spontaneously breathed room air (FIO2 0.21). Postextubation the calculated venous admixture of patients who had received 50% oxygen (0.20 +/- 0.03 [SD]) was significantly (p less than .01) greater than that calculated for patients who received lower oxygen concentrations (0.13 +/- 0.04). Consequently, the PaO2 of patients who had received 50% oxygen (60 +/- 5 torr) was significantly (p less than .03) lower than the PaO2 of patients who had received no more than 30% oxygen (66 +/- 7 torr). Thus, administration of 50% oxygen, supposedly nontoxic, to mechanically ventilated patients may cause impairment of pulmonary gas exchange after tracheal extubation. Although high concentrations of supplemental oxygen are sometimes required, unnecessary elevation of FIO2 is not likely to significantly increase oxygen delivery and may contribute to postextubation pulmonary dysfunction.

Perioperative complications of elective tracheostomy in critically ill patients.

This study was designed to examine prospectively the incidence of perioperative complications associated with elective tracheostomy in critically ill patients. An experienced surgeon and anesthesiologist participated in every tracheostomy procedure. In 81 procedures, there was no loss of airway control for greater than 20 sec, no airway obstruction, no blood loss exceeding 50 ml, and no aspiration. One patient (1.2%) had cardiovascular instability. During the next 48 h, two patients (2.4%) required wound packing to control hemorrhage but did not require blood transfusion and two patients (2.4%) had evidence of supraclavicular subcutaneous emphysema that was physiologically inconsequential. There was no perioperative mortality or major morbidity associated with the tracheostomy procedure. We conclude that, under controlled conditions, elective tracheostomy can be performed safely in critically ill patients.