Bo Brismar

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.

Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis

Pulmonary gas exchange and the development of atelectasis were studied in eight essentially lung‐healthy patients, awake and during halothane anaesthesia with mechanical ventilation. Gas exchange was evaluated by a multiple inert‐gas elimination technique and conventional blood‐gas analysis, and atelectasis was studied by computerized tomography (CT). Ventilation and lung perfusion were well matched in the majority of the patients when awake. In two patients there was low perfusion of poorly ventilated regions (low VA/Q). One patient had a shunt corresponding to 4% of cardiac output. None of the patients showed signs of atelectasis on the CT scans. After 15 min of anaesthesia, shunt had appeared in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. The major VA/Q mode was widened and ventilation of poorly perfused regions (high VA/Q) was noted in seven patients. Densities in dependent lung regions (interpreted as atelectasis) were seen on the CT scans in six patients. The extent of atelectasis was significantly correlated both to the magnitude of shunt (r = 0.93, P<0.01) and to the impairment of arterial oxygenation (r = 0.99, P<0.001). The findings indicate that atelectasis in dependent lung regions during halothane anaesthesia creates shunting of blood flow and that atelectasis is the major or sole cause of impaired gas exchange in the lung‐healthy, anaesthetized subject.

Atelectasis and lung function in the postoperative period.

Thirteen patients with healthy hearts and lungs, and with a mean age of 68 years, who were scheduled for lower abdominal surgery during isoflurane anaesthesia with muscular paralysis, were investigated with arterial blood gases, spirometry, pulmonary x‐ray and computed tomography (CT) of the chest before and during anaesthesia, as well as during the first 4 postoperative days. Before anaesthesia, lung function and gas exchange were normal in all patients. Pulmonary x‐ray and CT scans of the lungs were also normal. During anaesthesia, 6 of 13 patients developed atelectasis (mean 1.0% of intrathoracic transverse area in all patients). Two hours postoperatively, 11 of 13 patients had atelectasis and the mean atelectatic area was 1.8%. Pao2 was significantly reduced by 2.1 kPa to 9.8 kPa. On the first postoperative day, the mean atelectasis was unaltered (1.8%). None of the atelectasis found on CT scanning could be detected on standard pulmonary x‐ray. Forced vital capacity (FVC) and forced expired volume in 1 s (FEV1) were significantly decreased to 2/3 of preoperative level. Pao2 was significantly reduced to less than 80% of the preoperative level (mean 9.4 kPa). There were significant correlations between the atelectatic area and the impairment in FVC, FEV1, and Pao2. Spirometry and blood gases improved during the succeeding postoperative days, and atelectasis decreased. No patient suffered from pulmonary complications, as judged from clinical criteria and pulmonary x‐ray, in contrast to the findings of atelectasis in 85% of the patients by computed tomography.

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.

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.

Constitutional factors promoting development of atelectasis during anaesthesia.

The extent of atelectasis was correlated to constitutional factors in 38 patients who underwent computed tomography prior to and during general anaesthesia with halothane. All patients but two developed atelectasis in dependent regions of both lungs immediately after induction of anaesthesia prior to surgery. The transverse area of the densities ranged from 0 to 27 cm2, and there were no significant differences between patients of different age or sex, or with different smoking habits. A significant linear regression was found between Brocas index and the area of the densities, and also between an index describing the shape of the thorax and the density area. Thus, patients who were overweight and/or had a low and wide thorax tended to develop more extensive atelectasis during anaesthesia. This finding might partly explain why overweight patients develop postoperative pulmonary complications more often than non‐obese patients.

Central and regional hemodynamics during acute hypovolemia and volume substitution in volunteers.

OBJECTIVES To study the central and regional hemodynamics and oxygen consumption during acute hypovolemia and volume replacement with crystalloid and colloid solutions. DESIGN Prospective, randomized, laboratory investigation. SETTING Clinical physiology department at a university hospital. SUBJECTS Eighteen healthy male volunteers, between 21 and 35 yrs of age (mean 26). INTERVENTIONS Catheters were inserted in the cubital vein, brachial artery, pulmonary artery, thoracic aorta, right hepatic vein, and left renal vein for measurements of systemic arterial and pulmonary arterial pressures, total and central blood volumes, extravascular lung water, and the splanchnic (liver) and renal blood flow rates. The exchange of respiratory gases was measured, using the Douglas bag technique. Measurements were made before and after a venesection of 900 mL and again after the subjects had been randomized and received volume replacement with either 900 mL of Ringers acetate solution 900 mL of albumin 5%, or 900 plus 900 mL of Ringers solution. MEASUREMENTS AND MAIN RESULTS Withdrawal of 900 mL of blood decreased cardiac output and the splanchnic and renal blood flow rates by between -16% and -20%. The oxygen uptake decreased by 13% in the whole body, while it remained unchanged in the liver and kidney. The systemic and pulmonary vascular resistances increased, while the extravascular lung water decreased. Autotransfusion of fluid from tissue to blood was indicated by hemodilution, which was most apparent in subjects showing only a minor change in peripheral resistance. Cardiac output, blood volume, and systemic vascular resistance were significantly more increased by infusion of 900 mL of albumin 5% than by 900 mL of Ringers solution. However, infusion of 1800 mL of Ringers solution increased the extravascular lung water and the pulmonary arterial pressures to significantly above baseline, while no significant difference from baseline was found after 900 mL of Ringers acetate solution. CONCLUSIONS Withdrawal of 900 mL of blood induces similar reductions in cardiac output as in the splanchnic and renal blood flow rates. A fluid shift from the extravascular to the intravascular fluid compartment might restore up to 50% of the blood loss. Optimal volume substitution with Ringers solution can be effectuated by infusing between 100% and 200% of the amount of blood lost.

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.