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Biomedical subjects

M C Stock

Publications and source records attributed to M C Stock.

At least 19 recordsLinked to original sources
PubMed1996

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.

Animals↗
PubMed1995

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.

Adult↗
PubMed1995

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.

Adult↗
PubMed1992

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.

Acute Disease↗
PubMed1991

Airway pressure release ventilation during acute lung injury: a prospective multicenter trial.

OBJECTIVE: To evaluate the feasibility of airway pressure release ventilation (APRV) in providing ventilatory support to patients with acute lung injury of diverse etiology and mild-to-moderate severity. DESIGN: Prospective, multicenter, nonrandomized crossover trial. SETTING: ICUs in six major referral hospitals. PATIENTS: Fifty adult patients with respiratory failure requiring mechanical ventilation and positive end-expiratory airway pressure. INTERVENTIONS: After optimization of continuous positive airway pressure (CPAP), conventional ventilation and APRV were administered sequentially for 30 mins. During APRV, the CPAP level and airway pressure release level were adjusted to prevent hypoxemia, while the degree of ventilatory support was adjusted by altering the frequency of pressure release. MEASUREMENTS AND MAIN RESULTS: Circulatory and ventilatory pressures, arterial blood gases and pH, heart rate, and respiratory rate were measured. Alveolar ventilation was augmented adequately in 47 of 50 patients by APRV. Adjustment of APRV required an increase in mean CPAP from 13 +/- 3 (SD) to 21 +/- 9 cm H2O and a release pressure of 6 +/- 5 cm H2O. This airway pressure pattern produced a mean airway pressure comparable to that pressure achieved during conventional ventilation. Failure of APRV in three patients could be attributed to an inadequate level of CPAP or an inadequate APRV rate. While maintaining oxygenation of arterial blood and circulatory function, APRV allowed a substantial (55 +/- 17%; p less than .0001) reduction in peak airway pressure compared with conventional positive pressure ventilation adjusted to deliver a comparable or lower level of ventilatory support. CONCLUSIONS: APRV is a feasible alternative to conventional mechanical ventilation for augmentation of alveolar ventilation in patients with acute lung injury of mild-to-moderate severity.

Adult↗
PubMed1989

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.

Adult↗
PubMed1988

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.

Adult↗
PubMed1988

Transtracheal ventilation with oscillatory pressure for complete upper airway obstruction.

Another study documented that percutaneous transtracheal ventilation with a special 3.5-mm I.D. cannula was possible in experimental complete upper airway obstruction (CAO) using Ambu-assisted ventilation. The effects of ventilation during CAO by occlusion of the endotracheal tube was evaluated by use of a portable oscillatory pressure device (POPD) attached to a 10-g (I.D. 2.4 mm) angiocath catheter inserted through the tracheal wall. Eight pigs were anesthetized and ventilated with the POPD for 15 minutes after CAO with a mean peak airway pressure of 14 cm H2O and continuous positive airway pressure of 5-7 cm H2O, tidal volume below 100 ml, and a rate below 0.5 Hz. A Venturi delivered an FIO2 of 0.68-0.92. All eight showed markedly stable blood gases and cardiovascular parameters (heart rate and systemic and pulmonary arterial pressures). A similar trend was obtained in a separate group of four pigs ventilated with an Ambu bag for 30 minutes; however, the PO2 was lower. In the control group, asphyxia after CAO produced cardiorespiratory failure in every animal in less than 6 minutes. Low-frequency ventilation with a POPD for CAO ensures adequate gas exchange using a standard transtracheal catheter of only 2.4 mm I.D.

Airway Obstruction↗
PubMed1988

Oxygen consumption during spontaneous ventilation with acute lung injury in anesthetized pigs.

Acute lung injury causes a restrictive pulmonary defect, decreases lung compliance, and increases the work of breathing. We wished to determine the oxygen cost of the increased elastic work of breathing associated with acute lung injury. Extracorporeal venous circulation with a membrane lung was used to extract CO2 and to induce apnea in 14 anesthetized pigs. Data were collected during 4 experimental states: during spontaneous ventilation and apnea when the animals' lungs were normal, and after acute lung injury developed because of oleic acid administration. Acute lung injury decreased lung compliance from 101 +/- 79 (mean +/- SD) to 52 +/- 25 ml/cm H2O (p less than 0.04), and increased the elastic work of breathing from 700 +/- 590 to 1,060 +/- 630 ml.cm H2O (p = 0.01). During spontaneous ventilation, the increases in total O2 consumption and the O2 cost of breathing caused by acute lung injury were sufficiently small as to be undetectable, and, therefore, less than 3 to 4% of basal O2 consumption despite markedly increased elastic work and ventilatory power requirements. The increase in O2 consumption imposed by acute lung injury was small enough (less than 3 to 4% of total O2 consumption) that it appears to be clinically insignificant.

Acute Disease↗
PubMed1988

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.

Animals↗
PubMed1988

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.

Airway Resistance↗
PubMed1988

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.

Blood Gas Monitoring, Transcutaneous↗