Termination Of Mechanical Ventilation Research Articles

Effect of static lung expansion on pulmonary function following cardiopulmonary bypass in children

ObjectiveTo observe the effect of the lung-protective ventilation strategy, static lung expansion, during cardiopulmonary bypass (CPB) on pulmonary function and tracheal intubation time following cardiac surgery in children. MethodsA total of 48 child patients (aged 1–3) with ventricular septal defect (VSD) were enrolled, and all underwent CPB cardiac surgery for the first time. The patients were divided into two groups using the random number table method: the experimental group (Group A, n = 30) and the control group (Group B, n = 18). After terminating the mechanical ventilation during CPB, the adjustable pressure limiting valve of the anesthesia machine was adjusted in the experimental group to maintain the pressure of the breathing circuit at 5 cmH2O, such that both lungs remained in a static expansion state. In the control group, routine mechanical ventilation was terminated as usual. ResultsWhen static lung expansion with a continuous positive airway pressure of 5 cmH2O was employed in the VSD children during CPB, compared with termination of mechanical ventilation, the partial pressure of oxygen in the arterial blood increased, while the respiratory index decreased and the oxygenation index increased following the surgery. ConclusionIn child patients undergoing VSD reparation under CPB, lung injury occurs following the procedure, and the pulmonary oxygenation function and pulmonary oxygen diffusion function decrease. When static lung expansion of 5 cmH2O is performed during CPB, the improvement in lung function is better than that of apnea without lung expansion pressure.

Relationship of Laser-Doppler-Flow and coronary perfusion and a concise update on the importance of coronary microcirculation in donor heart machine perfusion.

Machine perfusion (MP) is a novel method for donor heart preservation. The coronary microvascular function is important for the transplantation outcome. However, current research on MP in heart transplantation focuses mainly on contractile function. We aim to present the application of Laser-Doppler-Flowmetry to investigate coronary microvascular function during MP. Furthermore, we will discuss the importance of microcirculation monitoring for perfusion-associated studies in HTx research. Porcine hearts were cardioplegically arrested and harvested (Control group, N = 4). In an ischemia group (N = 5), we induced global ischemia of the animal by the termination of mechanical ventilation before harvesting. All hearts were mounted on an MP system for blood perfusion. After 90 minutes, we evaluated the effect of coronary perfusion pressures from 20 to 100 mmHg while coronary laser-doppler-flow (LDF) was measured. Ischemic hearts showed a significantly decreased relative LDF compared to control hearts (1.07±0.06 vs. 1.47±0.15; p = 0.034). In the control group, the coronary flow was significantly lower at 100 mmHg of perfusion pressure than in the ischemia group (895±66 ml vs. 1112±32 ml; p = 0.016). Laser-Doppler-Flowmetry is able to reveal coronary microvascular dysfunction during machine perfusion of hearts and is therefore of substantial interest for perfusion-associated research in heart transplantation.

Respiratorentwöhnung – Definition und klinischer Kontext aus Sicht der Anästhesie

Independent from the mode of mechanical ventilation, particularly a quick termination of mechanical ventilation is essential for the weaning progress. Respirator-associated complications need to be early detected and treated. Thus it is important to know correspondent pathomechanisms as they have a crucial influence on the weaning process.To facilitate a holistic treatment approach for patients in prolonged weaning, a tight junction of intensive care within specialized units seems mandatory.

Hypothalamic-pituitary-adrenal axis dysfunction in critically ill patients with traumatic brain injury: incidence, pathophysiology, and relationship to vasopressor dependence and peripheral interleukin-6 levels.

To investigate hypothalamic-pituitary-adrenal axis function in patients requiring mechanical ventilation for traumatic brain injury and to assess the relation of hypothalamic-pituitary-adrenal axis abnormalities with vasopressor dependence and peripheral cytokine levels. Prospective study. General intensive care unit in a university teaching hospital. Forty patients (33 men and 7 women) with moderate to severe traumatic brain injury (mean age, 37 +/- 16 yrs) were studied the day after termination of mechanical ventilation (7-60 days after trauma). First, a morning blood sample was obtained to measure baseline cortisol, corticotropin, interleukin-6, and tumor necrosis factor alpha. Subsequently, 1 microg of synthetic corticotropin was injected intravenously, and 30 mins later, a second blood sample was drawn to determine stimulated plasma cortisol. Based on data derived from healthy volunteers, patients having stimulated cortisol levels <18 microg/dL were defined as nonresponders to the low-dose stimulation test. Thirty-one patients underwent also a human corticotropin releasing hormone test. In traumatic brain injury patients, mean baseline and low-dose stimulation test-stimulated cortisol levels were 17.2 +/- 5.4 microg/dL and 24.0 +/- 6.6 microg/dL, respectively. The median increment in cortisol was 5.9 microg/dL. Basal corticotropin levels ranged from 3.9 to 118.5 pg/mL. Six of the 40 patients (15%) failed the low-dose stimulation test. The human corticotropin releasing hormone test (performed in 26 responders and five nonresponders) revealed diminished cortisol release only in the low-dose stimulation test nonresponder patients. Corticotropin responses to corticotropin releasing hormone were consistent with both primary (three patients) and/or secondary (two patients) adrenal dysfunction. In retrospect, nonresponders to the low-dose stimulation test more frequently required vasopressors (6/6 [100%] vs. 16/34 [47%]; p =.02) and for a longer time interval (median, 0 vs. 293 hrs; p =.006) compared with responders. Furthermore, nonresponders had higher interleukin-6 levels compared with responders (56.03 vs. 28.04 pg/mL; p =.01), whereas tumor necrosis factor alpha concentrations were similar in the two groups (2.42 vs. 1.55 pg/mL; p =.53). Adrenal cortisol secretion after dynamic stimulation is deficient in a subset of critically ill patients with moderate to severe head injury. This disorder is associated with prior vasopressor dependency and higher interleukin-6 levels.

Association Between Reduced Cuff Leak Volume and Postextubation Stridor

Laryngotracheal injury or edema in the setting of intubation may narrow the upper airway and predispose toward postextubation stridor. The presence or absence of an audible airleak when the sealing balloon cuff of the endotracheal tube is deflated has been demonstrated to be a marker of laryngotracheal edema in high-risk patients. We hypothesized that (1) the volume of the cuff leak can be quantified in a general medical ICU population, and (2) the cuff leak volume can be correlated with likelihood of postextubation stridor. Within 24 h of both the initiation and termination of mechanical ventilation, the cuff leak volume, defined as the difference between the inspiratory tidal volume and the averaged expiratory tidal volume while the cuff around the endotracheal tube was deflated, was recorded. In 100 consecutive intubations, the preextubation cuff leak volume was 349 +/- 163 mL [mean +/- SD]). Overall, 6% of extubations were accompanied by postextubation stridor. The mean cuff leak volume measured within 24 h of planned extubation was significantly lower in those who subsequently developed stridor in comparison to those who did not (180 +/- 157 mL vs 360 +/- 157 mL; p = 0.012). The positive predictive value for postextubation stridor in the setting of a cuff leak less than 110 mL was 0.80, the predictive value for absence of postextubation stridor with a cuff leak volume greater than 110 mL was 0.98, and the specificity of the test was 0.99. No other demographic factors or indexes related to mechanical ventilation were significantly different between the two groups. A reduced cuff leak volume prior to extubation identifies a population at increased risk for postextubation stridor.

Apnoea following normocapnic mechanical ventilation in awake mammals: a demonstration of control system inertia.

1. Inhibition of inspiratory muscle activity from volume-related feedback during mechanical ventilation has been shown previously. To determine if this neuromechanical inhibition displays a memory effect, the duration of expiration immediately following cessation of mechanical ventilation was assessed in eight normal subjects. The subjects were passively mechanically ventilated via a nasal mask until the end-tidal CO2 (PET,CO2) was a minimum of 30 mmHg and inspiratory effort was no longer detected, as evidenced by stabilization of mouth pressure and disappearance of surface diaphragm EMG activity. The ventilator output was held constant at a mean tidal volume (VT) of 1.0 l and breath duration of 4.6 s and PET,CO2 was increased 1-1.5 mmHg/min (via increased inspired CO2 fraction, FI,CO2) until inspiratory muscle activity returned. The PET,CO2 at which activation first occurred was defined as the CO2 recruitment threshold (PCO2,RT). The mechanical ventilation protocol was repeated and the PET,CO2 increased 1-1.5 mmHg/min until it was a mean of 1.1 mmHg above spontaneous PET,CO2 and 3.6 mmHg below PCO2,RT. After 4-6 min of mildly hypercapnic mechanical ventilation, the mechanical ventilation was terminated. 2. Following termination of mechanical ventilation, the duration of the subsequent apnoea was 14.6 +/- 2.8 s (mean +/- S.E.M.) or 453 +/- 123% > spontaneous TE and 178 +/- 62% > the TE chosen by the subject during 'assist control' ventilation at VT = 1.0 l. 3. To test the hypothesis that the apnoea following cessation of mechanical ventilation was due to a vagally mediated memory effect, the study was repeated in five double-lung transplant patients with similar PCO2,RT to normal subjects. These pulmonary vagally denervated patients also displayed an apnoea (14.5 +/- 4.0 s) upon cessation of mechanical ventilation (at a PET,CO2 2.0 mmHg > eupnoea and 2.4 mmHg < PCO2,RT), that was 367 +/- 162% > spontaneous TE. 4. We also found significant apnoea in the awake dog immediately following mildly hypercapnic passive mechanical ventilation, and this was similar before and after bilateral vagal blockade (15.7 +/- 1.3 and 19.7 +/- 4.7 s, respectively). 5. We conclude that neuromechanical inhibition of inspiratory muscle activity, produced by passive mechanical ventilation at high VT, exhibits a memory effect reflected in TE prolongation, which persists in the face of substantial increases in chemoreceptor stimuli. This effect is not dependent on vagal feedback from lung receptors. 6. We hypothesize that this persistent apnoea represents an inherent 'inertia', characteristic of the ventilatory control system.(ABSTRACT TRUNCATED AT 400 WORDS)

Magnetic fields associated with anoxic depolarization in anesthetized rats

We have performed simultaneous measurements of the DC-magnetoencephalogram (DC-MEG) and DC-electrocorticogram (DC-ECoG) in rats (n = 6) subjected to 90 s of reversible anoxia. The onset of major shifts of electric and magnetic signals occurred at 52 ± 18 (S.D.) and 68 ± 14 (S.D.), respectively, and reached a peak at 83 ± 27 and 102 ± 19 (S.D.) s, respectively, after termination of mechanical ventilation. DC-ECoG signal deflections were always associated with DC-MEG deflections. The time of onset and peak signals in both DC-MEG and DC-ECoG changes caused by asphyxia were highly correlated ( r + 0.83, 0.94; P < 0.05, 0.001; respectively). Our observations suggest that the non-invasive technique of DC-MEG is reliable and may provide insight into the mechanisms of anoxic cerebral depolarization.

Fatal respiratory distress syndrome after prolonged mechanical ventilation: Its pathogenesis and prevention

Prolonged pulmonary atelectasis was shown to produce a highly lethal respiratory distress syndrome. Atelectasis with secondary hypoxemia occurred in open-chest animals ventilated for long periods with intermittent positive pressure (IPPV). These animals frequently died of progressive pulmonary insufficiency a few days after the period of thoracotomy and mechanical ventilation. Atelectasis did not occur in closed-chest animals subjected to long periods of IPPV and these animals did not manifest pulmonary insufficiency after the period of ventilation. Continuous positive-pressure ventilation (CPPV) prevented atelectasis in open-chest animals during prolonged mechanical ventilation and thoracotomy, and animals so treated developed postoperative pulmonary insufficiency infrequently. It is concluded that atelectasis, which occurs during IPPV in open-chest animals, if prolonged, leads to progressive, bilateral massive pulmonary consolidation and death a few days after closure of the chest and termination of mechanical ventilation. This frequently fatal respiratory distress syndrome does not occur if atelectasis is prevented during mechanical ventilation.