Improvement In Arterial Oxygenation Research Articles

Adult Respiratory Distress Syndrome: A Complication of Shock

ARDS is a complex type of respiratory failure that usually is a complication of a catastrophic critical illness, such as shock. Mortality is high, especially in patients with septic shock and multisystem failure. Mortality often is related to complications of refractory hypoxemia. Identifying patients at risk for developing ARDS and early recognition of ARDS are important so that treatment can be initiated to prevent the potentially lethal consequences of refractory hypoxemia. The nurse has an important role in collaborating with the physician and respiratory therapist to support the patient's oxygenation, ventilation, and tissue oxygen delivery system. The nurse is responsible for performing highly sophisticated assessment of clinical and hemodynamic parameters to evaluate the effectiveness of therapy. A key role of the nurse is anticipating, recognizing, and reporting to the physician complications of hypoxemia and complications of therapy that can lead to sepsis, airway trauma, or failure of other organ systems.

Cardiorespiratory Effects of Pressure Controlled Inverse Ratio Ventilation in Severe Respiratory Failure

Cardiorespiratory values were measured in nine patients with severe respiratory failure before and following initiation of pressure controlled inverse ratio ventilation (PC-IRV) at an inspiratory to expiratory ratio of 2:1. All patients showed increases in PaO2, with the mean PaO2 rising from 63 +/- 4 (mean +/- SEM) to 76 +/- 8 mm Hg. Peak inspiratory pressure fell from 44 +/- 4 to 39 +/- 2 cm H2O. There were no significant changes in any hemodynamic or oxygen metabolism variable associated with the institution of PC-IRV. In particular, no significant alteration in cardiac index, pulmonary artery pressures, oxygen delivery, oxygen consumption, or oxygen extraction ratio occurred with the use of PC-IRV. These results suggest that PC-IRV may be a useful ventilatory modality in the treatment of severe respiratory failure since it results in improvement in arterial oxygenation without any deterioration in hemodynamic or tissue oxygen metabolism parameters.

Coil embolization in the treatment of pulmonary arteriovenous malformations.

Twenty-eight pulmonary arteriovenous malformations in six patients were treated with coil embolization. The technique of embolization and the precautions taken to avoid complications are described. All patients had good relief of their symptoms and an improvement in arterial oxygenation. The observed complications were minor and our technique has now been modified to avoid these.

Mixtures of low molecular weight surfactant proteins and dipalmitoyl phosphatidylcholine duplicate effects of pulmonary surfactant in vitro and in vivo.

Pulmonary surfactant proteins SP-B and SP-C were isolated from lavage fluids of bovine lungs and recombined (lipid/proteins, 9/1, wt/wt) with dipalmitoyl phosphatidylcholine for testing in vitro and in surfactant-deficient adult rats. Using a pulsating bubble surfactometer, we found that inflation pressures of bubbles at minimum radii in these mixtures were 0.34 +/- 0.05 cm H2O (+/- SD, n = 24) after 1 min. These values were not affected by increasing amounts of surfactant protein relative to dipalmitoyl phosphatidylcholine (DPPC). Minimum inflation pressures were similar to those of modified bovine surfactant, surfactant Tokyo Akita (TA) (0.33 +/- 0.05 cm H2O, n = 7). In vivo testing was carried out in adult rats made surfactant deficient by repeated lavage and ventilated with 100% oxygen. Rats received tracheal instillations of either air, DPPC, DPPC/SP-B,C (9:1), or surfactant TA at 50 mg/kg body weight. Surfactant TA and DPPC/SP-B, SP-C mixtures resulted in similar immediate and sustained improvements in arterial oxygenation (308 +/- 66 torr, n = 10 and 312 +/- 101 torr, n = 6 at 30 min posttreatment) that were significantly greater than those of sham (76 +/- 24 torr, n = 17) and DPPC-treated rats (64 +/- 32 torr, n = 7). Rats treated with either DPPC/SP-B,C mixtures or surfactant TA showed similar postmortem static lung compliances (2.3 +/- 0.8 ml/cm H2O/kg, n = 8 and 1.9 +/- 0.4 ml/cm H2O/kg, n = 5, respectively) that were significantly larger than sham (1.3 +/- 0.3 ml/cm H2O/kg, n = 14) and DPPC-treated rats (1.2 +/- 0.2 ml/cm H2O/kg, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Ibuprofen on the Hypoxemia of Established Ethchlorvynol-Induced Unilateral Acute Lung Injury in Anesthetized Dogs

Nonsteroidal anti-inflammatory agents, given prior to induction of unilateral acute lung injury with ethchlorvynol (ECV) in anesthetized dogs, prevent the decreases in systemic oxygen tension (PaO2) which are observed when ECV is given alone. We investigated whether ibuprofen, administered after acute lung injury, would result in improvement in arterial oxygenation. In animals not receiving ibuprofen after unilateral acute lung injury with ECV, PaO2 decreased and venous admixture increased significantly from control values at all experimental time-periods. In those animals receiving ibuprofen, significant decreases in venous admixture were noted. The decrease in PaO2 after ECV administration was significantly less than that observed in animals that did not receive ibuprofen after acute lung injury (p less than 0.05). Ibuprofen had no effect on extravascular lung water. These results demonstrate that in an ECV model of acute lung injury the administration of ibuprofen, after the acute lung injury, results in significant decreases in venous admixture.

Role of Intravenous Nitroglycerin in the Treatment of Severe Pregnancy-Induced Hypertension Complicated by Pulmonary Edema

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 +/- 4 to 14 +/- 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from -10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p less than 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 +/- 4 to 33 +/- 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur.

Role of intravenous nitroglycerin in the treatment of severe pregnancy-induced hypertension complicated by pulmonary edema

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 ± 4 to 14 ± 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from −10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p < 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 ± 4 to 33 ± 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur

Delayed respiratory failure during the treatment of myxedema coma.

Three male patients (aged 41, 71 and 65 years) with untreated severe hypothyroidism of long duration were in a state of coma. This had been preceded by respiratory symptoms accompanied by hypoxemia and hypercapnea. There were also various chest radiographic findings. All the patients were treated with mechanical ventilatory assistance, circulatory support and i. v. administration of high doses of l-triiodo-thyronine (T3) during the early period of treatment. None of the patients showed any serious cardiac ill-effects immediately or a few days following the intravenous administration of T3. In spite of the stabilisation of vital signs and improvement in arterial oxygenation, the patients remained in a comatous or semicomatous state for the first few days. During the second week, the condition of their lungs deteriorated and prolonged respiratory failure ensued with fever, rales, excessive bronchial secretion, homogeneous densities in the chest radiograms and persistent hypoxemia even though mechanical ventilatory treatment was continued. The implications of this delayed respiratory failure during the treatment of myxedema coma are discussed.

The effect of massive weight loss on arterial oxygenation and pulmonary function tests.

Pulmonary function tests (PFTs) and arterial oxygenation were studied 24 hours preoperatively and again at varying times (5 to 20 months) during the postoperative weight loss of 37 morbidly obese patients. Among PFTs, expiratory reserve volume (ERV) demonstrated the most significant (P less than 0.001) improvement with weight loss. No clinically relevant differences were found after weight loss in FEV1, FVC, or MMEF. In 11 patients whose arterial blood gases were sampled before and after weight loss, a significant correlation was demonstrated between change in ERV and change in Pao2 (r = 0.59, P less than 0.05) and P(A-a)o2 (r = 0.76, P less than 0.01). When weight loss is expressed as either change in body mass index (delta BMI) or as a change in percent of ideal weight (delta wt), there existed a weight loss threshold for improvement in arterial oxygenation. A delta BMI of greater than 20 or a delta wt more than 100 per cent resulted in a significant improvement in Pao2 (P less than 0.01) or P(A-a)o2 (P less than 0.05). These data suggest that morbidly obese patients do not meaningfully improve FEV1, FVC, or MMEF with massive weight loss. However, there is a significant improvement in ERV that directly correlates with improvement in both Pao2, and P(A-a)o2.

Arterial Oxygenation during Artificial Ventilation. The Effect of Airway Closure and of Its Prevention by Positive End-Expiratory Pressure

Airway closure and arterial blood gases were measured in 11 healthy subjects both before and during anaesthesia with artificial ventilation, prior to routine surgery. The functional residual capacity was then increased by positive end-expiratory pressure (PEEP), so that ventilation took place at a lung volume where no airway closure was present, and the effect on arterial oxygenation was again investigated. A significant increase in alveolar-arterial oxygen gradient occurred in the group of seven patients in whom airway closure within a tidal breath could be demonstrated during anaesthesia, but there was no significant change in the four patients in whom airway closure could not be demonstrated. There was no improvement in arterial oxygenation on increasing functional residual capacity (FRC) in either group. It may well be that this failure to improve oxygenation was due to a deleterious effect of PEEP on the circulation, even though the PEEP was the minimum required to abolish airway closure.

Hemodynamic factors influencing arterial hypoxemia in massive pulmonary embolism with circulatory failure.

Arterial hypoxemia is a common finding in acute pulmonary embolism, and its severity is generally assumed to be proportional to the extent of pulmonary artery obstruction. We studied blood gases (during room air breathing and 100% oxygen breathing) and hemodynamic data is seven patients with massive pulmonary embolism and circulatory failure. All measurements were made before and 30 minutes after medical therapy of shock. We observed that a low cardiac output state can result in a misleading improvement in arterial oxygenation during massive pulmonary embolism, and that an improved circulatory status resulting from medical therapy (including inotropic drug infusion with or without blood volume expansion) can paradoxically increase arterial hypoxemia. We conclude that severity of arterial hypoxemia may not reflect the severity of pulmonary artery obstruction in acute pulmonary embolism if shock is present.

Improvement in Arterial Oxygenation by Saralasin Infusion in Man

Simultaneous hemodynamic and blood gas measurements were performed in 26 hypertensive adults, who were cigarette smokers, before and after a 30-minute infusion of saralasin (5 microgram/kg/min) which is a highly specific competitive antagonist of angiotensin II (AII). The arterial pressure fell in nine, rose in seven and was unchanged in ten patients. The mean cardiac index for the entire group remained unchanged. Pulmonary arterial or wedge pressure, pulmonary vascular resistance, arterial PCO2 and pH did not change. Unrelated to the hemodynamic changes, the mean arterial oxygen pressure (PaO2) increased from 68.6 +/- 2.2 mm Hg to 73.9 +/- 2.1 mm Hg (P less than 0.001). In the absence of a significant increase in alveolar ventilation as indicated by an unchanged mean PCO2 and lacking a hemodynamic explanation, the mechanism for the rise in PaO2 is speculative at this stage. The possibility of an improvement in the distribution of ventilataion by saralasin infusion is under investigation.

Effect of tolazoline in severe hyaline membrane disease.

Tolazoline hydrochloride was given as a pulmonary vasodilator to 20 preterm infants with severe hyaline membrane disease requiring mechanical ventilation who developed persistent severe hypoxaemia. The drug was only given when deterioration persisted despite changes in ventilation techniques and thus there were no control infants. A significant improvement in arterial oxygenation was observed, particularly in those infants without intracranial haemorrhage or pneumothroax. Nine of 10 infants who had an obvious clinical response to tolazoline survived, whereas only 2 survived out of 10 who failed to respond, both being subsequently shown to have pneumothoraces. There appears to be a place for the use of tolazoline in a severely hypoxaemic infant with hyaline membrane disease who is being ventilated and in whom arterial oxygenation cannot be improved by further increase in the inspired oxygen concentration or by alteration of ventilator settings, provided pneumothorax has been excluded.

Arterial Oxygenation During Artificial Ventilation: The Effect of Airway Closure and of its Prevention by Positive End‐Expiratory Pressure

Airway closure and arterial blood gases were measured in 11 healthy subjects both before and during anaesthesia with artificial ventilation, prior to routine surgery. The functional residual capacity was then increased by positive end-expiratory pressure (PEEP), so that ventilation took place at a lung volume where no airway closure was present, and the effect on arterial oxygenation was again investigated. A significant increase in alveolar-arterial oxygen gradient occurred in the group of seven patients in whom airway closure within a tidal breath could be demonstrated during anaesthesia, but there was no significant change in the four patients in whom airway closure could not be demonstrated. There was no improvement in arterial oxygenation on increasing functional residual capacity (FRC) in either group. It may well be that this failure to improve oxygenation was due to a deleterious effect of PEEP on the circulation, even though the PEEP was the minimum required to abolish airway closure.

Management of severe respiratory insufficiency due to Pneumocystis carinii pneumonitis in immunosuppressed hosts: the role of continuous negative-pressure ventilation.

Continuous negative-pressure therapy was used to assist ventilation in 19 spontaneously breathing patients, 6 months to 17 years of age, who developed progressive respiratory insufficiency (arterial PO2 less than 70 mm Hg despite a fraction of inspired O2 larger than or equal to 50 per cent) due to Pneumocystis carinii pneumonitis. Within 1 hour of therapy, arterial PO2 increased from a mean +/- SE of 61.9 +/- 3.7 to 75.4 +/- 7.0 mm Hg (P less than 0.05) and, by 6 hours, to 79.9 +/- 4.7 mm Hg (P less than 0.005). In the 14 survivors, these improvements were sustained and, within 24 hours, permitted a decrease in inspired O2 concentration from a mean +/- SE of 50.4 +/- 1.2 per cent to 40.1 +/- 1.6 per cent (P less than 0.005). By contrast, in nonsurvivors, O2 requirements could not be decreased significantly despite increases in negative pressure. Improvements in arterial oxygenation were associated with decreases in alveolar-arterial PO2 differences in all patients; however, significant decreases occurred only with pressures of -8 to -12 cm H2O. Higher negative pressures were ineffective and usually produced pulmonary air leak. Since the introduction of continuous negative-pressure therapy as a means of assisting ventilation in management of progressive respiratory insufficiency, the over-all survival rate among patients with Pneumocystis carinii pneumonitis at this institution has increased from 69 to 89 per cent.

Effects of continuous positive airway pressure on lung mechanics of babies after operation for congenital heart disease.

The effect of continuous positive airway pressure (CPAP) on lung mechanics was investigated in 12 babies after operation for severe congenital heart disease. At the time of study all babies were receiving or being weaned from ventilatory support and had abnormally low lung volume or compliance. During CPAP there was a fall in the pulmonary resistance which, with a slight decrease in minute ventilation, resulted in a significant decrease in the work of breathing. It is suggested that lowering the oxygen cost of breathing may contribute to the improvement in arterial oxygenation seen when CPAP is used.

The Use of Spontaneous Ventilation with Constant-Positive Airway Pressure in the Treatment of Salt Water Near Drowning

Constant-positive airway pressure with spontaneous ventilation was successfully used in treatment of a patient who had suffered near-drowning in salt water. The patient was able to maintain adequate respiratory mechanics, although oxygenation without end-expiratory pressure was severely impaired. The rapid improvement in arterial oxygenation obviated the need for mechanical ventilation in this patient. It is suggested that the simplest modality of effective therapy should be used in such patients.

Editorial Expression

This article represents a report of a very well managed, difficult problem in respiratory therapy. In a patient with a large bronchopleural fistula, the adult respiratory distress syndrome developed. When the need for high inspired oxygen concentrations continued despite the dehydration regimen, the authors felt that positive end-expiratory pressure was necessary to lower inspired oxygen concentrations. The use of positive end-expiratory pressure was noted to decrease the volume of the lung on the side of the fistula and to increase the apparent functional residual capacity of the other lung. It may be postulated that with increasing atelectasis of the pneumonic lung there was an increased resistance to blood flow through that lung and a shift of Wood flow to the aerated lung with its lower vascular resistance. The technique was valid in this patient at least temporarily, in that the inspired oxygen concentrations could then be lowered and the changes of the adult respiratory syndrome improved. An important question must be asked in this type of situation as to the effect upon the pneumonic lung itself of increased atelectasis and decreased blood flow. It is probable that decreased aeration and diminished perfusion tend to increase the severity of pneumonitis within the lung by impaired cellular metabolism, and decreased tissue antibiotic levels. This technique then, if used in the critical situation, must be used with the understanding and knowledge that it is probably a two-edge sword; improvement in arterial oxygenation which occurs must be balanced against the probable deleterious effects upon the collapsed lung itself.

Acute respiratory distress syndrome in pancreatitis.

Analysis of the records of 50 consecutive patients with acute pancreatitis admitted to a general hospital showed that 9 (18%) had diffuse pulmonary infiltrates. Dyspnea and shock were common, and arterial hypoxemia was invariably present in all patients studied (arterial PO2, 44 to 56 mm Hg). Five of the nine patients died with severe hypoxemia despite oxygen therapy. Postmortem studies showed pulmonary congestion and diffuse nonspecific pneumonitis without evidence of bacterial infection. One of the survivors had a gradual improvement in arterial oxygenation over a 4-week period. Pulmonary physiological testing 3 months later showed normal findings, except for a diffusing capacity of 50% of predicted. These findings indicate that severe hypoxemia is common in acute pancreatitis, but with appropriate care the lung disease is largely reversible. Possible pathophysiological mechanisms include injury to the lung by pancreatic enzymes, destruction or impaired synthesis of pulmonary surfactant, and pulmonary congestion secondary to myocardial failure.