Congestive Atelectasis Research Articles

Acute respiratory distress syndrome

There are several medical conditions that directly or indirectly lead to pulmonary destruction or acute lung injury or Acute Respiratory Distress Syndrome e.g. Sepsis, Inhalation of harmful substances, severe pneumonia, Head, chest, or another major injury, Pancreatitis (inflammation of the pancreas), massive blood transfusions and burns. Due to some incidences involved in the etiology of ARDS and limited information about the epidemiology, recognition, management, and less significant results regarding patients with acute respiratory distress syndrome (ARDS), shows intense research on ARDS is needed. From an earlier time, this syndrome has been given many names, including congestive atelectasis, traumatic adult respiratory distress syndrome and shock lung. Recently, the new definition of ARDS has been published, and this definition suggested severity-oriented respiratory treatment by introducing three levels of severity consistent with PaO2/FiO2 and positive end-expiratory pressure. Lung-protective ventilation is still the key to a better outcome in ARDS. ARDS is said to a selection of etiologies, carries high morbidity, mortality (10to 90%), and financial cost. This review is an attempt to compile all aspects of the management of ARDS.

Mechanical Ventilation in ARDS: Quo Vadis?

Contemplating the future should be grounded in history. The rise of post-polio ICUs was inextricably related to mechanical ventilation. Critically ill patients who developed acute respiratory failure often had "congestive atelectasis" (ie, a term used to describe ARDS prior to 1967). Initial mechanical ventilation strategies for treating this condition and others inadvertently led to ventilator-induced lung injury. Both injurious ventilation and later use of overly cautious weaning practices resulted from both limited technology and understanding of ARDS and other aspects of critical illness. The resulting misperceptions, misconceptions, and missed opportunities took decades to rectify and in some instances still persist. This suggests a reluctance to acknowledge that all therapeutic strategies reflect the historical period in which they were developed and the corresponding limited understanding of ARDS pathophysiology at that time. We are at the threshold of a revolutionary moment in critical care. The confluence of enormous clinical data production, massive computing power, advances in understanding the biomolecular and genetic aspects of critical illness, and the emergence of neural networks will have enormous impact on how critical care is practiced in the decades to come. Therefore, it is imperative we understand the long-crooked path needed to reach the era of protective ventilation in order to avoid similar mistakes moving forward. The emerging era is as difficult to fathom as our current practices and technologies were to those practicing 60 years ago. This review explores the history of mechanical ventilation in treating ARDS, describes current protective ventilation strategies, and speculates how ARDS management might look 20 years from now.

David Ashbaugh reminisces

In 1964, while I was working as codirector of the University of Colorado's (Boulder, CO, USA) first intensive care unit (ICU), I saw my first case of what turned out to be acute respiratory distress syndrome. At the time, I was puzzled about a number of symptoms that I hadn't previously recognised. If the patient had been admitted in the time before intensive care wards and respirators, they would have died without the attending physician knowing why and how. This particular patient was one of the first admitted to a new ICU set up by Dr Thomas Petty and myself. We had just finished residencies in medicine and surgery, respectively, and had lobbied for and obtained the necessary funds and space. We had one primitive respirator to use on patients with respiratory failure. The patient was admitted as a surgical trauma patient to my service, with multiple fractures after an automobile accident. Despite major blood loss, he soon stabilised and had a normal chest x-ray despite a few broken ribs. Over the course of 48 h, he developed respiratory distress and was intubated and put on the respirator, which was run from the hospital wall oxygen supply on a pressure-controlled basis. Despite 100% oxygen and maximum pressure, his condition worsened and fluffy infiltrates appeared in both lungs. He proceeded to die of respiratory failure. The rapid onset fluffy infiltrates, increasing pressures that required us to ventilate the patient, and falling oxygenation puzzled me as I had not seen this in patients before. Over the following months I saw a couple of similar cases, and went to the library to see what I could find. At the time there was only one reported case of congestive atelectasis following trauma. I consulted with our pathologists and infectious disease specialists and we did find hyaline membranes and alveolar haemorrhage in our patient. Some months later I had borrowed an Engstrom respirator from our anaesthesia department. It was a volume-controlled device and superior to anything we had on our ICU. When a 12-year-old boy presented in the emergency room on a Saturday morning, I was called to come down as he was in severe respiratory distress and coughing up blood after being backed over by a pickup truck. I did an immediate tracheostomy and transferred him to the paediatric care unit. Tom Petty had recently obtained a new blood gas analyser and I learned how to operate it. I spent the morning running up and down four flights of stairs and watching the patient's arterial blood gas deteriorate as we suctioned more and more blood from his tracheotomy. He was attached to the new respirator and I noticed, off to the right hand side, a red dial labelled “end expiratory pressure”. I wondered if this might help and dialled in a moderate amount. Within minutes the bleeding slowed and then stopped and the arterial blood gas returned to normal limits. Over the next few days he was weaned from the respirator and made a complete recovery. While this was obviously a case of traumatic pulmonary contusion, it was still a case of severe respiratory distress and positive end expiratory pressure was clearly an effective treatment. Within 2 years we had collected 12 cases, which included three patients treated with positive end expiratory pressure. Getting the paper published was a struggle, and after four rejections from US-based journals, we submitted it to The Lancet, which not only accepted the paper, but published it on the basis of in-house review within 6 weeks. For the first description of ARDS see Lancet 1967; 290: 319–23 For the first description of ARDS see Lancet 1967; 290: 319–23

What Is the Acute Respiratory Distress Syndrome?

It has been known for decades that shock and sepsis can cause a syndrome of acute respiratory failure with characteristics of non-cardiogenic pulmonary edema. Over the years, this syndrome has been given a number of names, including congestive atelectasis, traumatic wet lung, and shock lung. In 1967 the modern counterpart to this syndrome was described and subsequently called the "acute respiratory distress syndrome" (ARDS). This syndrome results from lung injury and inflammation. As with inflammation elsewhere, ARDS is accompanied by many cellular and molecular processes, some of them specific to the syndrome, others perpetuating the syndrome, and others inactivating the by-products of inflammation. Since no specific clinical sign or diagnostic test has yet been described that identifies ARDS, its diagnosis is based on a constellation of clinical, hemodynamic, and oxygenation criteria. Current ARDS treatment is mainly supportive, since these patients frequently have coexisting conditions. Although in 1994 a new standard ARDS definition was accepted, that definition failed to standardize the measurement of the oxygenation defect and does not recognize different severities of pulmonary dysfunction. Based on current evidence there is a need for a better definition and classification system that could help us to identify ARDS patients who would be most responsive to supportive therapies and those unlikely to benefit because of the severity of their disease process. This paper examines our current understanding of ARDS and discusses why the current definition may not be the most appropriate for research and clinical practice.

M.T. Pepper Jenkins introduces Ringer's lactate to treat shock

M.T. Pepper Jenkins was one of the team that introduced balanced salt solutions (in those days, Ringer's Lactate) to the resuscitation of traumatic shock. The revolutionary proposal is one of the most important innovations in the modern care of the surgical patient. Before 1950, surgeons and physiologists felt that salt solutions were contraindicated in surgical patients because they did not excrete a sodium load. Anesthetized patients were given small amounts of D5W, and if blood loss was excessive, they were given transfusions of whole blood. The turning point came in 1950 when Jenkins reported a series of critical patients in hemorrhagic shock, who received D5W and whole blood for resuscitation. They developed high hematocrits, stiff lungs and pulmonary failure, called “congestive atelectasis.” Jenkins theorized that congestive atelectasis could be prevented if Ringer's Lactate was given with the blood. Over the next 30 years, Shires demonstrated the deficit of extracellular fluid, which occurs in hemorrhagic shock in dogs and humans, and the acute sequestered edema space that results from trauma. This work established the efficacy for the use of balanced salt solutions in shock. Salt solutions were not contraindicated, rather they are indicated and, in fact, life saving. Salt solutions are now used all over the world for the treatment of shock and have saved millions of lives. Our understanding of surgical fluid therapy has changed forever; and Jenkins could be compared to Copernicus who suggested that the earth and other planets rotate around the sun, changing the way we think about the universe.

Modern ideas about the structural and functional features of the "shock lung"

At present, mechanical and thermal injuries play an important role in the structure of mortality and lethality of the most able-bodied population. This is largely due to the development of multisystem or multiple organ failure after shock damage [20, 24]. One should agree with the opinion of Yu. Shuteu et al. [21] that among the vital organs, the damage of which is of decisive importance in the evolution of shock, the lungs have a primary role. According to numerous literature data, the involvement of the lungs in the pathological process increases the possibility of death in various types of shock from 25.5% to 85-90% [15, 34]. The totality of structural and functional changes in the lung that occur after exposure to the body of extreme factors is designated in the literature by various terms, most often as "acute respiratory failure syndrome", which in foreign literature corresponds to the name "adult respiratory distress syndrome", and in our country - "adult respiratory distress syndrome"(ARDS). In the literature, there are also such definitions of this condition as "wet (wet) lung", "water lung", "perfusion lung syndrome", "respiratory disorders syndrome", "Da Nang lung", "congestive atelectasis", "shock lung" or "lung with shock, etc. Such an abundance of terms is caused by the often contradictory approach of researchers to the assessment of morphological and functional changes that occur in the lungs at various stages of extreme conditions.

Acute respiratory failure induced by mechanical pulmonary ventilation at a peak inspiratory pressure of 40 cmH20

The effects of high pressure mechanical pulmonary ventilation at a peak inspiratory pressure of 40 cmH(2)O were studied on the lungs of healthy newborn pigs (14-21 days after birth). Forty percent oxygen in nitrogen was used for ventilation to prevent oxygen intoxication. The control group (6 pigs) was ventilated for 48 hours at a peak inspiratory pressure less than 18 cmH(2)O and a PEEP of 3-5 cmH(2)O with a normal tidal volume, and a respiratory rate of 20 times/min. The control group showed few deleterious changes in the lungs for 48 hours. Eleven newborn pigs were ventilated at a peak inspiratory pressure of 40 cmH(2)O with a PEEP of 3-5 cmH(2)O and a respiratory rate of 20 times/min. To avoid respiratory alkalosis, a dead space was placed in the respiratory circuit, and normocarbia was maintained by adjusting dead space volume. In all cases in the latter group, severe pulmonary impairments, such as abnormal chest roentgenograms, hypoxemia, decreased total static lung compliance, high incidence of pneumothorax, congestive atelectasis, and increased lung weight were found within 48 hours of ventilation. When the pulmonary impairments became manifest, 6 of the 11 newborn pigs were switched to the conventional medical and ventilatory therapies for 3-6 days. However, all of them became ventilator dependent, and severe lung pathology was found at autopsy. These pulmonary insults by high pressure mechanical pulmonary ventilation could be occurring not infrequently in the respiratory management of patients with respiratory failure.

Bacteremia

Pulmonary effects, lung clearance, and tissue retention of blood-borne Pseudomonas aeruginosa were compared in dogs (n = 5) and pigs (n = 5) during continuous 6-hour intravenous infusion of 1.2(10(9)) bacteria/min/20 kg. Control pigs received an equal volume of sterile saline. In contrast to controls, experimental pigs developed pulmonary artery (PA) hypertension (mean, 30 +/- SE 3; baseline, 17 mm Hg) and pulmonary failure manifested by hypoxemia (mean PaO2, 49 +/- 4; baseline, 78 +/- 2 mm Hg; p less than 0.001), increased intrapulmonary shunting (40 to 50%), noncardiogenic pulmonary edema, and congestive atelectasis, a pattern of pulmonary failure very similar to sepsis-induced ARDS in humans. In dogs, PA pressures wee unchanged from baseline, no edema was detected, and comparable hyperventilation was associated with an increase in PaO2 from 77 +/- 4 (baseline) to 87 +/- 2 mm Hg (p less than 0.001). Tissue retention of viable blood-borne organisms in pigs was greatest in the lungs. In dogs, lung retention was minimal and greatest tissue retention occurred in the liver and spleen. We conclude that both lung clearance of blood-borne organisms and bacteremia-induced pulmonary failure are quite host dependent.

Pulmonary and systemic hemodynamics during hemorrhagic shock in baboons.

The pulmonary and systemic hemodynamic response to four hours of hemorrhagic shock and resuscitation has been studied in 17 baboons using both open and closed chest models. No pulmonary artery (PA) hypertension occurred during shock or resuscitation except for an increase in lft ventricular end diastolic pressure (LVEDP) secondary to intravascular volumee overload with Dextran. Pulmonary vascular resistance (PVR) increased during shock but returned to control levels with reinfusion of shed blood and correction of acidosis. PVR was moderately elevated following reinfusion of shed blood if acidosis was not corrected or if volum resuscitation was inadequate. No increase in gradients occurred between PA pressure and left atrial (LA) pressure or LVEDP and there was no gradients between small pulmonary vein and LA pressure. Arterial PO2 uniformly increased during shock and remained at or above control levels of reinfusion. Gross or histologic evidence of "congestive atelectasis" or "shock lung" was not observed. These observations suggest that in the subhuman primate, hemorrhage alone does not produce significant injury to the lung during shock or the immediate postresuscitation interval. Hemorrhage alone did not produce changes in the lung which would result in increased pulmonary microvascular hydrostatic pressure following appropriate resuscitation.

Prevention of pulmonary insufficiency through prophylactic use of PEEP and rapid respiratory rates

This study evaluated the effectiveness of prophylactic positive end-expiratory pressure (PEEP) rapid respiratory rates (RRR), and high tidal volume (HTV) in prevention of congestive atelectasis. Measurements of pulmonary hemodynamics, mechanics, gas exchange, functional residual capacity (FRC), pathology, and cinemicroscopy were performed in 45 anesthetized dogs subjected to hemorrhagic hypotension. Randomly, the animals received control ventilation, HTV (20 ml. per kilogram), RRR (32 breaths per minute), or PEEP (5 cm. of water). Carbon dioxide was added as needed to maintain normocapnia. Control and HTV animals showed characteristic changes of congestive atelectasis (capillary congestion, stasis, interstitial edema, periarterial hemorrhage, alveolar edema, and hemorrhage). These microscopic and cinemicroscopic changes were prevented by PEEP and RRR and correlated with decreased physiological shunting (PEEP 10 percent, RRR 13 percent, HTV 22 percent; p less than 0.01) in the postshock phase. PEEP increased FRC by 40 percent (p less than 0.02) and reduced the pulmonary artery--small pulmonary vein gradient (PA-SPV), suggesting a direct effect on the capillary bed. RRR did not affect FRC but minimized the SPV-LA gradient. This effect on the pulmonary venules theoretically could be mediated by stimulating lymphatic flow, thereby decreasing interstitial edema. Thus PEEP and RRR are beneficial when used prophylactically but may work by widely differing mechanisms.

Regional lung function following prosthetic hip replacement surgery.

With a Xenon133 radiospirometric technique the regional lung function was evaluated before and after prosthetic hip arthroplasty performed in the lateral decubitus position with either respirator-controlled neuroleptic anesthesia or epidural anesthesia with spontaneous breathing. Regional lung function measured in a supine position 1, 20 and 72-96 hours postoperatively revealed a reduction of the perfusion, ventilation and volume of ventilated alveoli on the dependant lung. The reduction was most pronounced immediately postoperatively, especially following respirator-controlled anesthesia. There was also an increase of pulmonary blood volume and a decrease of total lung volume in this group. The changes of lung function are probably caused by congestive atelectasis, secondary to impaired ventilation of the dependent lung. Peroperatively induced microembolism might have potentiated the effect.

Role of serotonin and serotonin antagonist on pulmonary hemodynamics and microcirculation in hemorrhagic shock

Previous studies showed that pulmonary pathological changes after hemorrhagic shock are similar to those after continuous (2 hours) serotonin infusion. Both conditions produce congestive atelectasis, interstitial and intra-alveolar edema and hemorrhage, and red cell aggregation. Studies in 25 dogs compared pulmonary hemodynamics during 2 hours of hemorrhagic hypotension (40 mm. Hg) with methysergide (serotonin antagonist), without methysergide, and with serotonin (75 mcg. per kilogram per minute) alone. During serotonin infusion in normovolemia, both pulmonary artery (PA) and pulmonary vein wedge (PVW) pressure rose. The pulmonary arteriolar and small pulmonary venous (SPV) constriction were statistically and physiologically significant. Pretreatment with methysergide prior to hypovolemia prevented the SPV pressure rise. Lung changes, grossly, microscopically, and by cinemicroscopy, were greatly reduced by administration of methysergide. These results suggest that serotonin—possibly released by the hypoxic intestine, hypoxic brain, or unstable platelets—plays a significant role in the pulmonary changes secondary to hypovolemic hypotension.

Physiologic effects of fluid therapy after pulmonary contusion

Summary The physiologic effects of fluid infusions given after pulmonary contusion were studied. Rapid infusion of blood, saline, or both produced an impulsive increase in pulmonary blood flow and pressure, particularly in the normal lung. A fall in normal lung resistance allows the pressure to reach the capillaries, resulting in leakage of blood and fluid into the normal lung (congestive atelectasis). Animals given rapid infusions suffered a shunt (Q s /Q t ) fraction larger than that of contused lung blood flow and more severe hypoxemia than did the controls. Hypotension followed by blood and saline administration did not alter lung function compared with saline infusion alone. It was suggested that some of the progression of pulmonary contusion as seen clinically and radiologically is due to damage in the normal lung. Monitoring of the pulmonary artery pressure during fluid administration after pulmonary contusion may be helpful in preventing further lung damage.

Factors influencing the measurement of pulmonary extravascular water

The change in pulmonary extravascular water calculated from indicator-dilution curves recorded by 125RISA and 131iodoantipyrene was compared to the weighed lung water in five groups of dogs. Four of these groups were kept hypotensive for 2 hr by hemorrhage, then reinfused with blood. They then received isoproteranol, methylprednisolone, phenoxybenzamine, or no drug. A fifth group was anesthetized for 4 hr, but kept normotensive. Hypotension, or prolonged anesthesia caused a recruitment of pulmonary capillaries in spite of a decreased cardiac output. This recruitment was decreased by isoproteranol or methylprednisolone and was unaffected by phenoxybenzamine. The recovery of RISA decreased during the course of all experiments. This decrease may be due to segmental areas of venous obstruction. Only in the group of animals receiving phenoxybenzamine after hypotension were the typical changes of congestive atelectasis seen.

Role of the atrial myocardium in the pathogenesis of the "shock lung".

Autotransplantation of one lung in dogs has been shown to protect the transplanted lung following hypovolemic and reinfusion of blood from the changes of congestive atelectasis referred to as shock In an attempt to elicit the factor responsible for this protection, ten dogs underwent sectioning and reanastomosis of the left atrial myocardium to interrupt the or extension of atrial myocardium onto the pulmonary veins. No protection was observed as determined by differential compliance and oxygen uptake, as well as by histologic studies. Our conclusion was that defunctionalization by interruption of the neuromuscular control of the throttle valve surrounding the ostia of the pulmonary veins did not protect against the congestive atelectasis of the lung.

Pulmonary arterial occlusion and surfactant production in humans.

Excerpt Local congestive atelectasis is a common occurrence with pulmonary infarction (1); its pathogenesis, however, is unclear. A prime role has been assigned to ischemic anoxia and subsequent reactive hyperemia from collateral bronchial arterial flow (2-5). The demonstration that pulmonary surfactant is secreted by alveolar epithelial cells (6) has raised the possibility that the altered metabolism of these cells may also be a factor. The purpose of this report is to examine the surface activity in extracts of human lungs involved with emboli and to attempt to relate these findings to the pathologic anatomic changes in the lung. MATERIALS AND METHODS

ACUTE RESPIRATORY DISTRESS IN ADULTS

The respiratory-distress syndrome in 12 patients was manifested by acute onset of tachypnœa, hypoxæmia, and loss of compliance after a variety of stimuli; the syndrome did not respond to usual and ordinary methods of respiratory therapy. The clinical and pathological features closely resembled those seen in infants with respiratory distress and to conditions in congestive atelectasis and postperfusion lung. The theoretical relationship of this syndrome to alveolar surface active agent is postulated. Positive end-expiratory pressure was most helpful in combating atelectasis and hypoxæmia. Corticosteroids appeared to have value in the treatment of patients with fat-embolism and possibly viral pneumonia.

EXTRACORPOREAL CIRCULATION, PULMONARY COMPLIANCE, AND PULMONARY SURFACTANT

R espiratory insufficiency may occur after cardiopulmonary bypass and present a serious postoperative problem. Tracheostomy and the use of mechanical respiratory assistance have been helpful in some patients. In others, the clinical and pathological picture has been characterized by congestive atelectasis, and postmortem studies of lung tissue have disclosed significant decreases in pulmonary surface activity. 4 This study was carried out to determine the effect of extracorporeal circulation upon the surface active characteristics of normal dog lung and upon the pulmonary pressure-gas volume relationship.

Clinical Manifestations and Treatment of Congestive Atelectasis

As a complication of the clinical course of disease, injury, or operation, the sudden and unanticipated onset of dyspnea, tachypnea, and cyanosis has achieved a well-deserved respect for serious portent and need for immediate and effective treatment. It is unfortunate, therefore, that accurate diagnosis of the causative factor or factors responsible for such disasters can be considerably more difficult to achieve than simple recognition that "something has gone wrong," so dramatically manifested by the initial symptoms. For surgical patients, additional difficulty in diagnosis may be superimposed by the intangibles of anesthesia, operation, serious trauma, and errors in parenteral fluid administration. Also, the diagnostic problem is not made easier by the variety of complex disturbed physiologic processes responsible for the principal signs and symptoms of acute cardiopulmonary insufficiency: (1) cyanosis; (2) tachypnea; (3) dyspnea; (4) tachycardia; and (5) hypotension. Congestive atelectasis is a descriptive term applied to an acute form of

CONGESTIVE ATELECTASIS IN LUNGS OF RABBITS AND OTHER ANIMALS SUBJECTED TO THE ACTION OF LOW BAROMETRIC PRESSURE

1. In rabbits, guinea‐pigs, rats, cats, and a dog subjected to the action of low barometric pressure, congestive lung atelectasis, of varying extent, has been found at post‐mortem examination.2. Experiments on rabbits exposed to decreased partial pressures of oxygen at different barometric pressures have shown that there is no relation between the incidence of congestive atelectasis and partial pressure of oxygen. The animals dying of anoxia at ground level or at barometric pressures between 500 and 300 mm. Hg showed all the usual lung changes but no congestive atelectasis.3. The animals decompressed from 3 or 5 atmospheres pressure to ground level also did not exhibit this lung change. There was no relation between the rate of decompression from the normal to low barometric pressures and the incidence or extent of congestive atelectasis.4. A direct relation between the level of decompression (300‐100 mm. Hg) and the incidence and extent of atelectasis was found, and it was concluded that the absolute rarefaction of air was the prime cause of congestive atelectasis formation.5. An increase of intra‐pulmonary pressure maintained in animals at low barometric pressures prevented lung atelectasis formation.6. The results of experiments of Hanson and Sjöstrand on the formation of lung atelectasis under the influence of different factors decreasing lung capacity at ground level are confirmed.7. The possible mechanism responsible for the lung atelectasis formation under the influence of low barometric pressure is discussed.We are very grateful to Professor I. de Burgh Daly for providing laboratory facilities and for his constant interest and advice. Our thanks are also due to Dr. Catherine Hebb and Dr. W. Missiuro for their help in carrying out some of the experiments. The expenses of this work were partially covered by a grant from the Polish Air Medical Council to J. Fegler.