In young, healthy people the alveolar–arterial PO2 difference (A-aDO2) is small at rest, but frequently increases during exercise. Previously, investigators have focused on ventilation/perfusion mismatch and diffusion abnormalities to explain the impairment in gas exchange, as significant physiological intra-pulmonary shunt has not been found. The aim of this study was to use a non-gas exchange method to determine if anatomical intra-pulmonary (I-P) shunts develop during exercise, and, if so, whether there is a relationship between shunt and increased A-aDO2. Healthy male participants performed graded upright cycling to 90% VO2max while pulmonary arterial (PAP) and pulmonary artery wedge pressures were measured. Blood samples were obtained from the radial artery, cardiac output (Q) was calculated by the direct Fick method and I-P shunt was determined by administering agitated saline during continuous 2-D echocardiography. A-aDO2 progressively increased with exercise and was related to Q (r = 0.86) and PAP (r = 0.75). No evidence of I-P shunt was found at rest in the upright position; however, 7 of 8 subjects developed I-P shunts during exercise. In these subjects, point bi-serial correlations indicated that I-P shunts were related to the increased A-aDO2 (r = 0.68), Q (r = 0.76) and PAP (r = 0.73). During exercise, intra-pulmonary shunt always occurred when A-aDO2 exceeded 12 mmHg and Q was greater than 24 l min−1. These results indicate that anatomical I-P shunts develop during exercise and we suggest that shunt recruitment may contribute to the widened A-aDO2 during exercise.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2004.069302

Intra-pulmonary shunt and pulmonary gas exchange during exercise in humans

We have compared the cardiorespiratory effects of an inspiratory: expiratory (I:E) ratio of 4:1 with a ratio of 1:2 in 10 adult patients requiring intermittent positive pressure ventilation (IPPV) for acute respiratory insufficiency. Further comparisons were made with IPPV with positive end-expiratory pressure (PEEP) which was adjusted to achieve an equal external end-expiratory volume (EEEV) to that produced by the 4:1 ratio, as determined by respiratory inductive plethysmography, and with an I:E ratio that only changed the EEEV minimally (IRV-min). Percentage pulmonary shunt (Qs/Qt) was reduced equally with PEEP and with the 4:1 I:E ratio but both patterns reduced cardiac output and oxygen delivery. IRV-min also reduced Qs/Qt significantly but had no effect on cardiac output so that oxygen delivery was increased. The dead space to tidal volume ratio (VD/VT) during IPPV-4:1 and IRV-min was reduced significantly when compared with that during IPPV-1:2. The clinical implications of the findings suggest that for some ITU patients, a modest increase in I:E ratio to between 1.1:1 and 1.7:1 may produce better gas exchange without significantly effecting the cardiac output.

/pdf/inverse-ratio-ventilation-compared-with-peep-in-adult-38szge2zv2.pdf

Inverse ratio ventilation compared with PEEP in adult respiratory failure

The pulmonary function of 49 patients admitted to the trauma services of Parkland Memorial Hospital was studied primarily in terms of volume function and blood-gas exchange. The incidence of fulminant pulmonary failure was low (three out of 49 or 6%). There was no evidence that shock without concomitant direct pulmonary injury increased the incidence of significant pulmonary dysfunction. Factors that predisposed the injured patient to pulmonary dysfunction were ( a ) direct thoracic or pulmonary injury, ( b ) sepsis, ( c ) aspiration of gastric contents, ( d ) head injury, and ( e ) fat embolization. The factor that appeared to jeopardize the patient's normal lung function most was sepsis. Almost all septic patients had defects in compliance and failed to maintain an adequate arterial oxygen pressure. A substantial number of severely injured patients required mechanical respiratory assistance to maintain normal pulmonary function.

Pulmonary response to major injury.

The Human Lung

Cardiac output was varied in 6 normal dogs and in 12 dogs with oleic acid induced pulmonary oedema by inducing hyper- and hypovolaemia produced by either transfusing or bleeding 15–20 ml of blood per kg body weight from the normovolaemic state. In normal dogs, a reduction in cardiac output of 42% was accompanied by a reduction in intrapulmonary shunt (Qs/Qt) from 9.8 to 6.4%. With induced pulmonary oedema, a 35% reduction in cardiac output was accompanied by a fall in Qs/Qt from 29 to 21.6%. In another series of experiments, mixed venous oxygen saturation was varied independently of cardiac output by means of veno-venous shunting of blood through a disc oxygenator. Decreasing SvO2 from 70 to 50% in normal lungs caused a decrease in QS/QT from 10.1 to 7.9% whilst in pulmonary oedema a decrease in Sv02 from 59.3 to 32.2% produced a decrease in Qs/Qt from 10.1 to 7.9% whilst in pulmonary oedema a decrease in SvO2 from 59.3 to 32.2% produced a decrease in Qs/Qt from 28.8 to 25.7%.

The effect of change in cardiac output on intrapulmonary shunting

SUMMARY Changes in cardiorespiratory function resulting from haemorrhage and overtransfusion were measured in forty-seven dogs during controlled ventilation. In the animals bled to a mean arterial pressure of 70 mm Hg there were significant reductions in arterial Pco2, carbon dioxide output and oxygen consumption, cardiac output and total venous admixture. In the animals transfused to a mean central venous pressure of 15 mm Hg there was a significant fall in total thoracic compliance and arterial Po3 and significant increases in the alveolar-arterial Po3, difference and carbon dioxide output.

The cardiorespiratory effects of haemorrhage and overtransfusion in dogs

SUMMARY Changes in cardiorespiratory function resulting from the use of three different inspiratory: expiratory ratios (1:2, 0.5:2.5, and 2:1) have been studied in normo-, hypo- and hypervolaemic dogs. Deadspace/tidal volume ratio increased slightly with the 0.5:2.5 ratio in all the states of blood volume but the changes were not statistically significant. There was a significant increase in arterial-alveolar Pco 2 difference on the 0.5:2.5 ratio in the hypervolaemic state and there was a significant reduction in the Pco 2 difference with the 2:1 ratio in the normovolaemic state. There was a significant reduction in arterial Po 2 and a significant increase in venous admixture on the 0.5:2.5 ratio in the hypervolaemic state. Cardiac output was reduced after haemorrhage and increased after overtransfusion but there were no significant changes resulting from changes in the I: E ratio within each state of blood volume.

The effects of variations in inspiratory: expiratory ratio on cardiorespiratory function during controlled ventilation in normo-, hypo- and hypervolaemic dogs

SUMMARY The cardiorespiratory effects of intravenous infusions of isoprenaline (3 and 12 μg/min) were studied in eighteen mechanically ventilated dogs. Isoprenaline produced an increase in cardiac output, carbon dioxide output and oxygen consumption and a non-respiratory acidosis. In six dogs minute volume was kept constant so that arterial Pco2 increased. These dogs developed a marked increase in total venous admixture, most of which was due to an increase in ventilation/perfusion inequality, In tyhe remaining two groups of dogs arterial Pco2 was kept constant by increasing tital volume or respiratory frequency. Isoprenaline produced a smaller increase in total venous admixture in these dogs but the increase in right-to-left shunt was approximately the same in all three groups of dogs. In another six dogs the addition of carbon dioxide to the inspired gas produced no change in venous admixture.

A.E. Wightman

Papers

The cardiorespiratory effects of haemorrhage and overtransfusion in dogs

The effects of variations in inspiratory: expiratory ratio on cardiorespiratory function during controlled ventilation in normo-, hypo- and hypervolaemic dogs

The cardiorespiratory effects of intravenous isoprenaline in mechanically ventilated dogs