L. Tokics

Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis.

Twenty patients (23–76 yr) were studied with regard to lung tissue changes prior to and following induction of general anesthesia with muscular relaxation, and another four subjects were studied for a longer period awake. The transverse thoracic area and the structure of the lung tissue were determined by computerized tomography. No abnormalities in the lung tissue were noted before anesthesia. Within 5 min after induction, including muscular relaxation, all subjects had developed crest-shaped changes of increased density in the dependent regions of both lungs. They were largest in the most caudal segment (4.8 ± 0.8% of the transverse lung area, mean ± SE) and smaller in the cephalad exposures (3.4 ± 0.7% of the transverse area). The size of the densities showed no correlation to age. The densities did not increase after a further 20 min of anesthesia and were not affected by the inspiratory oxygen fraction. When the subjects were moved from the supine to the lateral position, the crest-shaped densities disappeared in the nondependent lung and remained in the dorsal part of the dependent lung. The application of positive end-expiratory pressure of 10 cmH2O eliminated or reduced the densities. The four awake subjects showed no lung densities after 90 min in the supine position. It is suggested that these crest-shaped densities represent atelectases, which develop by compression of lung tissue rather than by resorption of gas.

Lung Collapse and Gas Exchange during General Anesthesia: Effects of Spontaneous Breathing, Muscle Paralysis, and Positive End-expiratory Pressure

Lung densities (atelectasis) and pulmonary gas exchange were studied in 13 supine patients with no apparent lung disease, the former by transverse computerized tomography (CT) and the latter by a multiple inert gas elimination technique for assessment of the distribution of ventilation/perfusion ratios. In the awake state no patient had clear signs of atelectasis on the CT scan. Lung ventilation and perfusion were well matched in most of the patients. Three patients had shunts corresponding to 2–5% of cardiac output, and in one patient there was low perfusion of poorly ventilated regions. CT scans after 15 min of halothane anesthesia and mechanical ventilation showed densities in dependent lung regions in 11 patients. A shunt was present in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. Ventilation of poorly perfused regions was noted in nine patients, ranging from 1–19% of total ventilation. The magnitude of the shunt significantly correlated to the size of dependent densities (r = 0.84, P < 0.001). Five patients studied during spontaneous breathing under anesthesia displayed both densities in dependent regions and a shunt, although of fairly small magnitude (1.8% and 3.7%, respectively). Both the density area and the shunt increased after muscle paralysis. PEEP reduced the density area in all patients but did not consistently alter the shunt. It is concluded that the development of atelectasis in dependent lung regions is a major cause of gas exchange impairment during halothane anesthesia, during both spontaneous breathing and mechanical ventilation, and that PEEP diminishes the atelectasis, but not necessarily the shunt.

Functional Residual Capacity, Thoracoabdominal Dimensions, and Central Blood Volume during General Anesthesia with Muscle Paralysis and Mechanical Ventilation

Functional residual capacity (FRC), rib cage and abdominal dimensions (rc-ab), central blood volume (CBV), and extra vascular lung water (EVLW) were measured in six lung-healthy subjects awake and during halothane anesthesia, muscle paralysis, and mechanical ventilation. FRC was assessed by multiple breath nitrogen washout, rc-ab dimensions by computerized tomography, and CBV and EVLW by a double-indicator dilution technique (thermo-dye). During anesthesia, FRC decreased by 0.5 1 (17%). The cross-sectional chest area was reduced by 12–20 cm2, causing an approximate reduction in thoracic volume by 0.3 1. Concomitantly, the diaphragm was moved cranially by an average of 1.9 cm, diminishing the thoracic volume a further 0.5 1. The abdominal cross-sectional area did not alter significantly, despite the shift of the diaphragm. CBV decreased by 0.3 1. EVLW did not change significantly. It is concluded that the thoracic volume is reduced during halothane anesthesia, muscle paralysis, and mechanical ventilation as a result of cranial shift of the diaphragm and reduction in transverse area. The decrease in thoracic volume is accompanied by a reduction in FRC and a displacement of blood from the thorax to the abdomen, the transverse area of the latter thus being maintained despite the shift of the diaphragm.

CT-assessment of dependent lung densities in man during general anaesthesia.

Purpose: We aimed to describe the frequency of atelectasis occurring during anaesthesia, to describe the size and pattern of the atelectasis, and to standardise the method of identifying the atelectasis and calculate its area. Material and Methods: Patients (n=109) scheduled for elective abdominal surgery were examined with CT of the thorax during anaesthesia. Results: In 95 patients (87%) dependent pulmonary densities were seen, interpreted as atelectasis. Two different types of atelectasis were found — Homogeneous (78%) and non-homogeneous (9%). Attenuation values in histograms of the lung and atelectasis were studied using 2 methods of calculating the atelectatic area. Conclusion: On the basis of the present findings, we defined atelectasis as pulmonary dependent densities with attenuation values of —100 to +100 HU.

PHRENIC NERVE STIMULATION DURING HALOTHANE ANESTHESIA - EFFECTS ON ATELECTASIS

Background:Atelectasis formation during anesthesia may be due to loss of respiratory muscle tone, in particular that of the diaphragm. This was tested by tensing the diaphragm by phrenic nerve stimulation (PNS) and observing the effect on atelectasis. Methods:Twelve patients (mean age 48 yr) without preexisting lung disease were studied during halothane anesthesia. PNS was executed with an external electrode on the right side of the neck. Chest dimensions and area of atelectasis were studied by computed tomography of the chest. Results:Right-sided PNS against an occluded airway at functional residual capacity reduced the atelectatic area in the right lung from 5.1 to 3.8 cm2. The atelectasis was reduced to 1.1 cm2 after application of positive end-expiratory pressure (PEEP) of 10 cmH2O and large tidal volumes but increased to 2.5 cm2 within 1 min after discontinuation of PEEP. Commencement of PNS immediately after PEEP prevented the atelectasis from increasing, the mean area being 0.9 cm2. In seven patients, in whom the trachea was intubated with a doublelumen endobronchial catheter the atelectatic area was smaller during PNS with an open airway than during positive pressure inflation of the lung with the same volume as inspired during PNS (3.5 and 5.2 cm2, respectively. Conclusions:The findings indicate that contracting the diaphragm in the anesthetized subject reduces the size of atelectasis.

Atelectasis and Gas Exchange Impairment During Enflurane/ Nitrous Oxide Anesthesia

The development of atelectasis and effects on gas exchange during enflurane anaesthesia in nitrogen/oxygen or nitrous oxide/oxygen (inspired oxygen fraction 0.4) were studied in 16 lung-healthy patients (mean age 49 years). Awake, no subject displayed atelectasis as assessed by computed x-ray tomography of the thorax. Pulmonary gas exchange, studied by multiple inert gas elimination technique, and blood gases were normal. After 10 min of enflurane anaesthesia in nitrogen/oxygen, 14 of 16 subjects had developed atelectasis. After 30 min of enflurane anaesthesia in nitrogen/oxygen or nitrous oxide/oxygen, all patients had developed atelectasis, and a further increase was observed after 90 min of anaesthesia to approximately 5% of the intrathoracic area. There was no difference between the two anaesthesia groups. In the nitrogen group, shunt rose to a maximum of 5.8% at 30 min of enflurane anaesthesia, with a significant reduction to the initial anaesthesia level after 90 min of anaesthesia (3.4%). Perfusion of poorly ventilated lung regions (low VA/Q) averaged 4-5% and did not vary significantly during the anaesthesia. In the nitrous oxide group, shunt increased to 6.3% after 90 min of anaesthesia, and there was a parallel decrease in perfusion of low VA/Q regions. The findings suggest that besides prompt collapse of lung tissue during induction of anaesthesia, absorption of gas from closed-off or poorly ventilated regions takes place and further increases the atelectatic area.

Influence of Age on Atelectasis Formation and Gas Exchange Impairment During General Anaesthesia

We have studied the effects of anaesthesia on atelectasis formation and gas exchange in 45 patients of both sexes, smokers and nonsmokers, aged 23-69 yr. None of the patients showed clinical signs of pulmonary disease, and preoperative spirometry was normal. In the awake patient, partial pressure of arterial oxygen (PaO2) decreased with increasing age (P less than 0.001) and the alveolar-arterial oxygen partial pressure difference (PAO2-PaO2) increased with age (P less than 0.001). Shunt, assessed by the multiple inert gas elimination technique, was small (mean 0.5%) and uninfluenced by age. However, there was an increasing dispersion (log SD Q) of ventilation/perfusion ratios (VA/Q) and increasing perfusion of regions of low VA/Q (VA/Q less than 0.1) with increasing age (P less than 0.001 and P less than 0.05, respectively). No patient displayed any atelectasis as assessed by computed x-ray tomography of the chest. During inhalation anaesthesia (halothane or enflurane) with mechanical ventilation, 39 of 45 patients developed atelectasis and shunt. There was a strong correlation between the atelectatic area and the magnitude of shunt (r = 0.81, P less than 0.001). Atelectasis and shunt did not increase significantly with age, whereas log SD Q and perfusion of regions with low VA/Q ratios did (r = 0.55, P less than 0.001 and r = 0.35, P less than 0.05, respectively). Awake, the major determinant of PaO2 was perfusion of regions of low VA/Q ratios, which increased with age. During anaesthesia shunt influenced PaO2 most, low VA/Q being a secondary factor which, however, was increasingly important with increasing age, thus explaining the well-known age-dependent deterioration of arterial oxygenation during anaesthesia.

Atelectasis During Anaesthesia and in the Postoperative Period

Transverse sections of lung tissue were studied in patients by computerized tomography during anaesthesia and in the postoperative period. Eight patients were studied during intravenous (thiopentone) and six during inhalational (halothane) anaesthesia. The latter patients were studied during both spontaneous and mechanical ventilation. Five of the patients who underwent surgery for inguinal hernia and five patients in whom laparotomy was performed were studied 1 h and 24 h postoperatively. No patient showed any lung changes while awake preoperatively, and all patients developed dependent, crest-shaped lung densities within 5-10 min of anaesthesia. The densities comprised 3.4% of the lung volume in the caudal (basal) 5 cm of the lung tissue. No significant differences in the size and distribution of the densities were noted between spontaneous breathing and mechanical ventilation during anaesthesia, or between intravenous and inhalational anaesthesia. The densities remained in nine of ten patients 1 h postoperatively, and they remained in five of ten patients 24 h after anaesthesia. The densities are considered to be compression atelectases which may develop as a result of relaxation of the diaphragm. They may be important contributors to postoperative pulmonary complications.