J. Santesson

Breathing mechanics, dead space and gas exchange in the extremely obese, breathing spontaneously and during anaesthesia with intermittent positive pressure ventilation.

Breathing mechanics and gas exchange were studied in 10 extremely obese subjects (average weight 138 kg) prior to and during anaesthesia with mechanical ventilation. Breathing mechanics were analysed from measurements of transpulmonary pressure (during anaesthesia, trans‐chest wall pressure as well) inspiratory gas flow and tidal volume. Gas exchange was studied by analysing inspired and expired gas as well as arterial blood samples. The total dead space was deduced from the Bohr equation, and the division into anatomical and alveolar dead space was arrived at by capnography. The patients were anaesthetised with neurolept agents and ventilated with an air‐oxygen mixture. Lung compliance during spontaneous breathing was below normal and decreased further during artificial ventilation. Chest wall compliance measured during anaesthesia was within normal limits. Lung resistance was above normal during spontaneous breathing and increased further during mechanical ventilation. Total dead space was normal during spontaneous breathing and increased moderately during artificial ventilation, the increment coming mainly from alveolar dead space. A moderate hypoxaemia was recorded during spontaneous breathing, and the alveolar‐arterial oxygen tension difference was slightly elevated. During anaesthesia this difference was markedly greater. It is concluded that the most probable reason for the relative hypoxaemia is right‐to‐left shunting.

Ventilation-Perfusion Distribution During Inhalation Anaesthesia

Ventilation‐perfusion (V̇a/Q̇) ratios were studied by means of an inert gas elimination technique in healthy subjects with an average age of 51 years in the supine posture (a) when awake, (b) during inhalational anaesthesia, spontaneously breathing, (c) during mechanical ventilation, and (d) when a positive end‐expiratory pressure (PEEP) was applied. In the awake subject a bimodal distribution of V̇A/Q̇ was recovered in most patients, one mode centered around the ratio of 1 and another, smaller mode, within low V̇A/Q̇‐regions. Any shunt was less than 3% of cardiac output. With anaesthesia and spontaneous breathing, the low V̇A/Q̇ mode was reduced and the shunt increased to an average of 6.2%. With mechanical ventilation, the major V̇A/Q̇ mode was widened while the shunt was further increased in 4 of 10 subjects (mean 8.6%). With PEEP, the shunt was reduced and a new mode within high V̇A/Q̇‐regions appeared. The shunt and low V̇A/Q̇‐regions may be explained in terms of airway closure while the high V̇A/Q̇ mode with PEEP may be attributed to the development of a zone I.

Airway Closure and Distribution of Inspired Gas in the Extremely Obese, Breathing Spontaneously and During Anaesthesia with Intermittent Positive Pressure Ventilation

Airway closure (closing capacity, CC), FRC, total efficiency of ventilation (lung clearance index, LCI) and distribution of inspired gas (nitrogen washout delay percentage, NWOD) were determined by nitrogen washout techniques and arterial Po2 and Pco2 measured by standard electrodes in 10 extremely obese subjects, prior to and during anaesthesia and artificial ventilation. CC was normal, but because of small FRC, airway closure occurred within a tidal breath in 9 out of 10 subjects during spontaneous breathing, when awake. Po2 was reduced, the hypoxaemia correlating to the magnitude of airway closure. LCI was normal, but NWOD was borderline. During anaesthesia, CC was unaltered but FRC was further reduced, so that in nine subjects airway closure occurred above FRC and tidal volume together. A marked increase in relative hypoxaemia was recorded. LCI and NWOD rose, indicating less efficient and less even ventilation. It is concluded that airway closure reasonably explains the marked hypoxaemia in obese subjects during anaesthesia, and that it may also be the reason for the uneven distribution of inspired gas.

Ventilation and Perfusion of Each Lung during Differential Ventilation with Selective PEEP

Lung perfusion was studied in 10 patients (mean age 58 yr) in the lateral position during enflurane anesthesia. They were ventilated through a double-lumen endotracheal catheter: 1) by one ventilator with free distribution of ventilation between the lungs, with no (zero) end-respiratory pressure (ZEEP); 2) as above but with a general positive end-expiratory pressure (PEEP) of 9 cmH2O; or 3) by two ventilators with equal distribution of ventilation between the lungs and with a selective PEEP of 8 cmH2O to the dependent lung only. Total ventilation was on average 8 l/min (BTPS) throughout the study. During the first method, 34% of ventilation was distributed to the dependent and 66% to the nondependent lung. Cardiac output (thermodilution) was 4.5 l/min, 57% being distributed to the dependent lung as assessed by iv boli of Xenon 133. During the second method, ventilation was assumed to be distributed equally between the lungs. Cardiac output was decreased to 3.8 l/min, and the dependent lung received 81% of lung blood flow. During the third method, cardiac output was significantly greater than during the second method (4.1 l/min), 51% passing to the dependent lung. Peak and end-inspiratory airway pressures were 5-18 cm H2O lower during selective than during general PEEP. Arterial oxygen tension was significantly greater during the third method than during either of the other ventilator settings and the alveolar-arterial oxygen tension difference was almost halved compared with the first method. It is concluded that differential ventilation with selective PEEP improves ventilation-perfusion matching and thus oxygenation.

Hypoxic Pulmonary Vasoconstriction in the Human Lung: Effect of Repeated Hypoxic Challenges during Anesthesia

Six patients, ages 29–58 yr, were investigated during barbiturate and fentanyl anesthesia. After intubation with a double-lumen bronchial catheter, one lung was ventilated continuously with 100% O2, and the other was rendered hypoxic during three 15-min periods by ventilation with 95% N2 + 5% O2, with intervening 15-min periods of oxygen ventilation. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The first hypoxic challenge resulted in a 10% increase in cardiac output (QT) and a reduction in the fractional perfusion of the test lung from 57% to 31% of QT. The pulmonary artery mean pressure increased by 54%, and the vascular resistance of the test lung increased threefold. The venous admixture increased from 19% to 40% of QT, whereas the inert gas shunt remained unaltered at 15% (inert gases also being eliminated by nitrogen-ventilated areas). The arterial oxygen tension decreased from 353 mmHg to 79 mmHg. On resumption of the control state, central hemodynamics and gas exchange returned to the initial values. The second and third hypoxic challenges resulted in reductions in the fractional perfusion of the test lung to 35% and 37% of QT. All other variables were altered to the same degree as during the first challenge. The authors conclude that hypoxic challenge of one lung in an intravenously anesthetized human subject elicits a maximum vasoconstrictor response within the first 15 min, and this response cannot be potentiated by repeated challenges.

Airway Closure During Anaesthesia, and its Prevention by Positive End Expiratory Pressure

Airway closure, functional residual capacity (FRC) and the transpulmonary pressure volume relationship of each lung were studied in the anaesthetized subject in the supine and the left lateral positions. In the supine posture, FRC was of approximately the same size in each lung as was closing capacity (CC). CC exceeded FRC in either lung. In the left lateral position, FRC was increased by 0.91 in the non‐dependent lung and was reduced by 0.2 1 in the dependent lung, while CC was unaltered in either lung. Consequently, FRC exceeded CC in the non‐dependent lung and was further lowered beneath CC in the dependent lung. Airway closure did not occur in the non‐dependent lung until an average of 0.51 of gas had been expelled after the dependent lung had ceased to empty. The addition of positive end‐expiratory pressure (PEEP) in the range 0.5–2 kPa, increased FRC more in the non‐dependent than the dependent lung. The findings suggest that airway closure is evenly distributed in the horizontal level, while it has a discontinuous distribution between the dependent and non‐dependent lung. Moreover, the increase in lung volume caused by PEEP has a distribution that is by no means ideal for the purpose of countering airway closure.

Differential Ventilation in Acute Bilateral Lung Disease. Influence on Gas Exchange and Central Haemodynamics

Eight patients with acute respiratory failure (ARF) due to diffuse and rather uniform lung disease were intubated with a double‐lumen bronchial tube and ventilated in the lateral decubital position by two synchronized ventilators. Ventilation of each lung was individually adjusted to match the expected regional blood flow (differential ventilation). When ventilation with equal volumes (i.e. 50% of tidal volume to each lung) was performed, a 19% reduction of venous admixture (P<0.001) and a 22% increment in arterial oxygen tension (P<0.001) were seen. Comcomitantly, the cardiac output increased by 17% (P<0.001), to which a reduced pulmonary vascular resistance may have contributed. The net result was a 14% increment of the oxygen availability (P<0.001). An attempt to go further, giving 2/3 of the tidal ventilation to the dependent lung, was made on six of the patients. However, this ventilatory pattern did not further improve the gas exchange and also had detrimental effects on the haemodynamics. It is concluded that differential ventilation with equal tidal volumes in the lateral position can substantially improve gas exchange and central haemodynamics in patients with ARF due to diffuse lung disease.

Oxygen Transport and Venous Admixture in the Extremely Obese. Influence of Anaesthesia and Artificial Ventilation with and without Positive End‐Expiratory Pressure

Eight extremely obese patients (mean weight 136 kg) were studied when awake and breathing air, and during anaesthesia with controlled ventilation (oxygen fraction in inspirate (Fio2): 0.5). During anaesthesia, the patients were first studied with zero end‐expiratory pressure (ZEEP) ventilation. Then two different positive end‐expiratory pressures (PEEP) were applied, 10 cmH2O and 15 cmH2O2 in order to study the effect of an increase in functional residual capacity (FRC). Arterial oxygenation and oxygen availability, as well as cardiac output (Qt) and venous admixture (Qs/Qt) were studied. With the institution of anaesthesia and ZEEP, the alveolar arterial oxygen tension difference (P(A‐a)o2) rose from 3.5 ± 1.1 to 28.4 ± 2.6 kPa, and the oxygen availability fell from 1346 ± 222 to 1039 ± 239 ml/min, due to the additive effect of an increase in Qs/Qt from 10 ± 4 to 21 ± 5% and a fall in QT, from 7.7 ± 1.2 to 5.5 ± 1.1 l/min. With increasing levels of PEEP, despite a fall in P(A‐a)o2, there was a reduction in oxygen availability. This was due to simultaneous reduction in Qs/Qt and QT. At a PEEP of 15cmH2O, the P(A‐a)o2 was 21.2 ± 7.1 kPa, oxygen availability 862 ± 170 ml/min, Qs/Qt 13 ± 4 and QT 4.4 ± 0.6 I. It is concluded that PEEP ventilation significantly reduces Qs/Qt in extremely obese patients during anaesthesia and should be used in these patients if there is arterial hypoxemia despite a high Fio2

Distribution of inspired gas to each lung in anesthetized human subjects.

The distribution of ventilation in man during halothane anesthesia was studied in a two‐compartment lung model in which each lung was ventilated separately by means of a double‐lumen tracheal tube. Eight subjects were studied prior to scheduled surgery. Tidal volume distribution was even between the lungs in the supine position (horizontal distribution) as was distribution of dynamic lung compliance, resistance and dead space. The vertical distribution was assessed when the patient was in the left lateral position. Dependent dynamic lung compliance and dead space were lower and lung resistance was higher than in the non‐dependent lung. These factors favoured a non‐dependent lung ventilation and, moreover, caused a re‐distribution from dependent to non‐dependent lung during an end‐inspiratory pause (EIP), thus increasing the inhomogeneity of ventilation. The application of a positive end‐expiratory pressure (PEEP) of 10 cmH2O improved dependent ventilation and abolished redistribution between the lungs. In conclusion, uneven distribution of dynamic lung compliance and lung resistance causes inhomogeneous ventilation distribution, favouring the non‐dependent lung. An EIP enhances and a PEEP reduces the inhomogeneity of ventilation.

The Effect of Surgical Stress on Haemodynamics During Neurolept Anaesthesia

The influence of surgical stress on haemodynamics during neurolept anaesthesia (NLA) was studied in ten patients, while they were awake, under anaesthesia prior to surgery and peroperatively. Systemic arterial, pulmonary arterial, right atrial and pulmonary capillary wedge pressures, as well as cardiac output (Qt), arterial oxygen content and mixed venous oxygen content, were measured. Systemic and pulmonary vascular resistances, arterial‐venous oxygen content difference (AVD), oxygen consumption (vo2 and cardiac index (CI) were calculated.