Catherine S.H. Sassoon

Patient-ventilator asynchrony.

The basic mechanism of patient-ventilator asynchrony is the mismatching between neural inspiratory and mechanical inspiratory time. Alterations in respiratory drive, timing, respiratory muscle pressure, and respiratory system mechanics influence the interaction between the patient and the ventilator. None of the currently available partial ventilatory support modes are exempt from problems with patient-ventilator asynchrony. Ventilator triggering design in the trigger phase and the set variables in the post-trigger phase contribute to patient-ventilator interaction. The set inspiratory flow rate in the post-trigger phase for assist-control volume cycled ventilation affects patient-ventilator asynchrony. Likewise, the initial pressure rise time, the pressure support level, and the flow-threshold for cycling off inspiration for pressure support ventilation are important factors affecting patient-ventilator asynchrony. Current investigations have advanced our understanding in this area; however, its prevalence and the extent to which patient-ventilator asynchrony affect the duration of mechanical ventilation remain unclear.

Inspiratory work of breathing on flow-by and demand-flow continuous positive airway pressure

Continuous positive airway pressure (CPAP) breathing can be delivered using the demand-flow (DF) or continuous-flow (CF) system. A modified CF system, the flow-by (FB) system, operates with preset base-flow (BF) values between 5 and 20 L/min. The DF depends on changes in pressure for opening the pneumatic valve of the system (pressure sensitivity). In contrast, the FB depends on changes in flow (flow sensitivity). In six healthy male subjects, we determined the mechanical inspiratory work of breathing (WI, J/L) and the inspiratory work rate (J/min) on the DF and the FB systems at a BF of 5 and 20 L/min, at CPAP levels of 0, 5, and 10 cm H2O. In comparison to DF, on the FB system both WI and inspiratory work rate were significantly less at a CPAP of 10 cm H2O (p less than .01). This was most likely due to the smaller drop in airway pressure at the onset of inspiration with the FB system. Varying the BF values in the FB system had no effect on WI or inspiratory work rate.

Iatrogenic Pneumothorax: Etiology and Morbidity

The purpose of this study was to delineate the etiological factors for iatrogenic pneumothorax in the era of increased use of invasive procedures and to determine its impact on morbidity. Between 1983

influence of pressure- and flow-triggered synchronous intermittent mandatory ventilation on inspiratory muscle work

Objective: To determine the effect of pressure‐ and flow‐triggered synchronous intermittent mandatory ventilation on inspiratory muscle work. Design: Consecutive clinical, prospective, randomized trial. Setting: Medical intensive care unit (ICU) of a U.S. Veterans Affairs Medical Center. Patients: Eight patients recovering from acute respiratory failure of various etiologies. Interventions: Assist‐control, followed by randomized application of pressure‐ and flow‐triggered synchronous intermittent mandatory ventilation at 60%, 40%, 20% of the assist‐control rate, and flow‐triggered continuous positive airway pressure. A total of eight settings were maintained for 10 mins each. Measurements and Main Results: Total work rate (joules/min), inspiratory muscle work (joules/L), and pressure time‐product per breath (cm H2O.sec) were measured. During pressure‐ or flow‐triggered synchronous intermittent mandatory ventilation, total work rate increased as the mandatory rate was decreased. The method of ventilator triggering had a significant effect on the total work rate. With pressure‐triggered synchronous intermittent mandatory ventilation, the total work rate at 60% of the assist‐control rate was similar to that with assist‐control; whereas with flow‐triggered synchronous intermittent mandatory ventilation, this result was achieved at 40% of the assist‐control rate. At a machine support level of 20%, total work rate with pressure‐triggered synchronous intermittent mandatory ventilation was significantly greater than with flow‐triggered synchronous intermittent mandatory ventilation. The method of ventilator triggering had no significant effect on the inspiratory muscle work of the mandatory breaths. This finding was in contrast to the effect on inspiratory muscle work of spontaneous breaths. With pressure‐triggered synchronous intermittent mandatory ventilation, inspiratory muscle work of the spontaneous breaths was greater than with the flow‐triggered at machine support of 40% and 20%. With either pressure‐ or flow‐triggered synchronous intermittent mandatory ventilation, inspiratory muscle work of the mandatory breaths was not significantly different from that of the corresponding spontaneous breaths, except at the lower machine support levels with the pressure‐triggered synchronous intermittent mandatory ventilation. Pressure‐time product followed a trend similar to that of inspiratory muscle work. Conclusions: During synchronous intermittent mandatory ventilation, the method of ventilator triggering has a significant effect on the total work rate and inspiratory muscle work of the spontaneous breaths, particularly at lower machine support levels. Conversely, the method of ventilator triggering has no significant effect on inspiratory muscle work of the mandatory breaths. (Crit Care Med 1994; 22:1933–1941)

Breathing pattern during acute respiratory failure and recovery

The objective of this study was to compare the breathing pattern of patients who failed to wean from mechanical ventilation to the pattern during acute respiratory failure. We hypothesized that a similar breathing pattern occurs under both conditions. Breathing pattern, mouth occlusion pressure (P[0.1]) and maximum inspiratory pressure (P[I,max]) were measured in 15 patients during acute respiratory failure, within 24 h of the institution of mechanical ventilation, and in 49 patients during recovery, when they were ready for discontinuation from mechanical ventilation. The following indices were calculated: rapid shallow breathing index (respiratory frequency/tidal volume (fR/VT)); rapid shallow breathing-occlusion pressure index (ROP = P[0.1 x fR/VT]); P(0.1)/P(I,max); and effective inspiratory impedance (P[0.1]/VT/(inspiratory time (tI)). Patients who failed to wean (n=11) had a similar ROP,fR/VT and P(0.1)/P(I,max) to those with acute respiratory failure despite a significantly reduced P(0.1)/VT/tI, the value of which was comparable to that of patients who weaned successfully (n=38). The P(I,max) of patients who failed to wean was similar to that of patients who weaned successfully. We conclude that patients who failed to wean had a breathing pattern similar to that during acute respiratory failure, despite a reduced mechanical load on the respiratory muscles and a relatively adequate inspiratory muscle strength. This suggests that strategies that enhance respiratory muscle endurance may facilitate weaning.

PATIENT–VENTILATOR INTERACTIONS

Patient-ventilator synchrony is important in the management of the ventilator-dependent patient. Factors inherent to the patient and the ventilator influence patient-ventilator synchrony. Detection of patient-ventilator synchrony may require monitoring of airway pressure and flow waveforms.

Variability of cardiac output over time in medical intensive care unit patients

ObjectivesTo determine the amount of spontaneous variability of cardiac output over time in critically ill patients, and to determine the effect of mechanical ventilation on cardiac output variability over time. DesignCase series. SettingMedical intensive care unit in a Veterans Affairs Medical Center. PatientsTwenty-two patients with indwelling pulmonary artery flotation catheters were studied. Two patients were studied twice. InterventionsDuring a 1-hr time period in which no interventions were required or made, thermodilution cardiac output was determined at baseline and then every 15 mins for 1 hr. At each time point, five individual cardiac output measurements were made and a mean was computed. The covariables of heart rate, respiration rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, and temperature were also recorded at each time point. Measurements and Main ResultsThe variability of the five cardiac output measurements made at each time point was expressed by calculating for each patient a coefficient of variation of the measurements. The overall mean coefficient of variation of the measurements was 5.8%. The variability of the cardiac output measurements over time was expressed by calculating for each patient a coefficient of variation over time. The overall mean coefficient of variation over time was 7.7%. A subgroup of 15 “covariable stable‘’ patients (defined as those patients with covariables within ±5% of the mean covariable values during the hour) had a mean coefficient of variation over time of 6.4%, whereas “covariable unstable‘’ patients (with >±5% changes in any covariable) had a mean coefficient of variation over time of 9.9% (p < .05). Patients breathing spontaneously had a mean coefficient of variation over time of 10.1%, whereas mechanically ventilated patients had a mean coefficient of variation over time of 6.3% (p < .05). ConclusionsThe spontaneous variability of cardiac output should be considered when interpreting two cardiac output determinations made at separate times. Due to spontaneous variability alone, a patient with a baseline cardiac output of 10.0 L/min would be expected (95% confidence interval) to have a cardiac output range of 9.2 to 10.8 L/min if covariables were stable, and a range of at least 8.8 to 11.2 L/min if covariables were unstable. Patients who were mechanically ventilated displayed less variability than patients who were breathing spontaneously. (Crit Care Med 1994; 22:225–232)

Cardiac output from carbon dioxide production and arterial and venous oximetry.

ObjectiveTo determine cardiac output from measurements of CO2 production (&OV0312;co2), and arterial (Sao2) and mixed venous (S&OV0456;o2) oxygen saturations, using a modified Fick equation, in which cardiac output = &OV0312;co2/[k (Sao2 – S&OV0456;o2)], where k represents a constant. DesignA metabolic measurement cart was used to measure &OV0312;co2 and oxygen consumption (&OV0312;o2) at 3-min intervals. Sao2 and S&OV0456;o2 were measured via a pulse oximeter and a fiberoptic right heart catheter, respectively. The initial value of k for each study was determined from initial simultaneous measurements of thermodilution cardiac output, &OV0312;co2, Sao2, and S&OV0456;o2 via the equation k = &OV0312;co2/[cardiac output (Sao2 – Svo2)]. The value of k was assumed to remain constant for the entire study period. Thereafter, cardiac outputs calculated from k and the measurements of &OV0312;co2, Sao2, and S&OV0456;o2 were compared with the simultaneously obtained cardiac outputs determined by thermodilution. Similarly, cardiac outputs calculated from the traditional oxygen Fick equation, where cardiac output = &OV0312;o2/[13.4 × hemoglobin (Sao2 – S&OV0456;o2)], were compared with the simultaneously acquired cardiac outputs determined by thermodilution. SettingSurgical ICU in a Veterans Affairs Medical Center. PatientsSeven postoperative patients, mechanically ventilated using the intermittent mandatory ventilation mode, were studied over a mean period of 4 hrs. ResultsCardiac output (obtained from &OV0312;co2 and oximetry saturations) was closely related to thermodilution cardiac output: with linear regression showing r2 = .96 and standard error of the estimate = 0.59 L/min, n = 21; and, with bias and precision = 0.17 and 0.68 L/min, respectively. The traditional oxygen Fick cardiac output was also closely related to the thermodilution cardiac output (r2 = .81, standard error of the estimate = 1.46 L/min, n = 22; bias and precision = 0.31 and 1.46 L/min, respectively). ConclusionThe proposed method for calculating cardiac outputs solely from &OV0312;co2 and oximetry saturations yields results that correspond closely to thermodilution determined cardiac outputs. The method is simple and avoids the difficulties in the Fick method associated with accurate &OV0312;o2 measurement. This approach may be suitable for continuous cardiac output monitoring in critically ill patients.

Acute effects of high-dose methylprednisolone on diaphragm muscle function

The time‐ and dose‐dependent effects of acute high‐dose corticosteroids on the diaphragm muscle are poorly defined. This study aimed to examine in rabbits the temporal relationships and dose–response effects of acute high‐dose methylprednisolone succinate on diaphragmatic contractile and structural properties. Animals were assigned to groups receiving: (1) 80 mg/kg/day methylprednisolone (MP80) intramuscularly for 1, 2, and 3 days; (2) 10 mg/kg/day methylprednisolone (MP10, pulse‐dose) for 3 days; or (3) saline (placebo) for 3 days; and (4) a control group. Diaphragmatic in vitro force–frequency and force–velocity relationships, myosin heavy chain (MyHC) isoform protein and mRNA, insulin‐like growth factor‐1 (IGF‐1), muscle atrophy F‐box (MAF‐box) mRNA, and volume density of abnormal myofibrils were measured at each time‐point. MP80 did not affect animal nutritional state or fiber cross‐sectional area as assessed in separate pair‐fed groups receiving methylprednisolone or saline for 3 days. Compared with control values, MP80 decreased diaphragmatic maximum tetanic tension (Po) by 19%, 24%, and 34% after 1, 2, and 3 days (P < 0.05), respectively, whereas MP10 decreased Po modestly (12%; P > 0.05). Vmax and MyHC protein proportions were unchanged in both the MP80 and MP10 groups. Maximum power output decreased after 2 and 3 days of MP80. Suppression of IGF‐1 and overexpression of MAF‐box mRNA occurred in both MP groups. Significant myofibrillar disarray was also observed in both MP groups. The decline in Po was significantly associated with the increased volume density of abnormal myofibrils. Thus, very high‐dose methylprednisolone (MP80) can produce rapid reductions in diaphragmatic function, whereas pulse‐dose methylprednisolone (MP10) produces only modest functional loss. Muscle Nerve, 2008

Oxygen Fick and modified carbon dioxide Fick cardiac outputs

Objective: To compare cardiac outputs estimated from the classical oxygen Fick and modified CO2 Fick methods with thermodilution cardiac output. The modified CO2 Fick cardiac output was obtained by replacing the oxygen uptake (Vo2) in the Fick equation with the CO2 production (Vco2) divided by either an assumed or measured value of the respiratory exchange ratio or with an independently determined constant (Crit Care Med 1991; 19:1270‐1277). Design: Criterion standard study. Setting: The medical and surgical intensive care unit (ICU) in a Veterans Affairs Medical Center. Patients: A total of 17 patients (26 studies) and 11 surgical patients (13 studies), predominantly mechanically ventilated using the intermittent mandatory ventilation mode, were studied over a period of 4.3 hrs. Measurements: A respiratory gas exchange monitor was used to measure Vo2, Vco2, and respiratory exchange ratio at 3‐min intervals. Calculations were performed with arterial and venous oxygen saturations measured with both a laboratory cooximeter and bedside pulse and venous reflectance oximeters. In the oxygen Fick method, cardiac output was calculated from Vo2 together with arterial and venous oxygen saturations. In the modified CO2 Fick methods, cardiac output values were calculated from arterial and venous oxygen saturations with Vco2, divided by either: a) an assumed value of the respiratory exchange ratio equal to 0.8 for all patients (method 1); b) the patients measured value of the respiratory exchange ratio (method 2); or c) a constant, determined from an initial, simultaneous measurement of thermodilution cardiac output, Vco2, and oximetry saturations. Data were examined by linear regression analysis and bias and precision calculations. Main Results: Thermodilution cardiac output was more related to cardiac outputs calculated with the 3 modified CO2 Fick methods than to the oxygen Fick cardiac output. Thermodilution cardiac output was closely related to the modified CO2 Fick cardiac output calculated via method 3. For this method, with pulse and venous reflectance oximetry saturations, linear regression yielded an r2 = .85, a standard error of the estimate of 0.88 L/min (n = 111) and a bias and precision of 0.11 and 0.97 L/min, respectively. Thermodilution cardiac output was less closely related to oxygen Fick cardiac output, which, when calculated with pulse and venous reflectance oximetry saturations, yielded an r2 = .50, a standard error of the estimate of 1.47 L/min (n = 128), and a bias and precision of 0.01 and 1.85 L/min, respectively. Conclusions: We conclude from this study that thermodilution cardiac output is more closely related to cardiac output calculated from modified CO2 Fick methods than to oxygen Fick cardiac output. Since cardiac output calculated with the modified CO2 Fick method 3 obviates the difficulties associated with measuring Vo2 accurately and requires neither an assumption of nor measurement of the respiratory exchange ratio, method 3 may prove to be clinically useful for continuous cardiac output monitoring via oximetry in ICU patients. (Crit Care Med 1994; 22:86‐95)