Pulmonary collapse

The striking similarities between the cardiovascular, ventilatory, and respiratory physiological responses to inhaled irritants and allergens implies that the irritant-induced pulmonary chemoreflex comprises a subset of the more profound allergen-induced anaphylactic cardiovascular and pulmonary collapse. 

Prolonged exposure may cause pulmonary oedema Systemic symptoms may occur in 0.5 to 1 hr Rapid collapse, respiratory paralysis imminent Immediately fatal... 

Pharmacology. Lycorine was first examined by Morishima wl found it relatively non-toxic to mammals. Given per os or subcutaneous, to the dog or cat, it causes, in small doses, salivation and in large dos vomiting and diarrhoea. It has no special effect on the blood pressure death seems to be due to a generalised collapse. Post mortem —hyper m and ecchymoses in the stomach, intestine, pulmonary pleura and end... 

Pulmonary surfactant decreases surface tension of alveolar fluid. Reduced surface tension leads to a decrease in the collapsing pressure of the alveoli, an increase in pulmonary compliance (less elastic recoil), and a decrease in the work required to inflate the lungs with each breath. Also, pulmonary surfactant promotes the stability of the alveoli. Because the surface tension is reduced, the tendency for small alveoli to empty into larger ones is decreased (see Figure 17.2, panel b). Finally, surfactant inhibits the transudation cf fluid out of the pulmonary capillaries into the alveoli. Excessive surface tension would tend to reduce the hydrostatic pressure in the tissue outside the capillaries. As a result, capillary filtration would be promoted. The movement of water out of the capillaries may result in interstitial edema formation and excess fluid in the alveoli. 

The therapy for IRDS includes mechanical ventilation with continuous positive airway pressure. This maintains adequate ventilation and prevents airway collapse between breaths with the formation of atelectasis. Therapy also includes administration of exogenous pulmonary surfactant. Two types of surfactants are used to prevent and treat IRDS in the U.S. These include surfactants prepared from animal sources as well as synthetic surfactants. Exogenous pulmonary surfactants are administered as a suspension (in saline) through the endotracheal tube used for mechanical ventilation. 

Phosgene is very poisonous so insidious that it was used as a war gas in World War 1. One deep breath can cause immediate collapse and death, and as it is not irritating there is no gag reflex to prevent one from taking that deep breath. Doses which are not high enough to be immediately lethal may not be noticed at till at the time of exposure, yet lead to death within 24 hours. Sub-lethal doses cause pulmonary edema and serious respiratory disability again, the symptoms can appear well after an exposure which was hardly noticed. 

Respiratory effects are more likely to occur after inhalation exposure to high concentrations of chloroform. It has been demonstrated that chloroform has a destructive influence on the pulmonary surfactant (Enhoming et al. 1986). This effect is probably due to the solubility of phospholipids in the surfactant monolayer and can cause collapse of the respiratory bronchiole due to the sudden increase in inhalation tension. Immediate death after chloroform inhalation may be due principally to this effect in the lungs (Fagan et al. 1977). It is unlikely that exposure levels of chloroform in the general environment or at hazardous waste sites would be high enough to cause these severe respiratory effects. 

A liposomal formulation containing a surfactant, which usually coats the mucosa of the bronehi and prevents a collapse of the alveolar vesieles of the lung, has been developed for patients who suffer from infant respiratory distress syndrome (IRDS) or adult-aequired respiratory distress syndrome (ARDS). Premature babies often suffer IRDS before the development of a funetional lung surfaetant and pulmonary gas exehange. ARDS is also a life-threatening failure and loss of the lung function and is usually acquired by illness or accident. Clinieal trials with liposomal surfactant have proved to be effective in prophylaetie treatment of IRDS and ARDS. 

In a study of the mechanism whereby BordeteUa pertussis vaccine increased acute ozone toxicity in rats, Thompson ascribed the effects to /3-adrenergic blockade, and not to an immune-mediated response. It was further noted that both atropine and reserpine reduced mortality, whidi suggested that the acute lethal effects of ozone were due to shock and circulatory collapse, rather than pulmonary edema. 

Animal experiments were undertaken to test the relationship 235 guinea pigs exposed to asbestos dusts were found to have asbestosis but no cancer (Vorwald and Karr, 1938), whereas only two pulmonary carcinomas were reported among ten surviving mice after 240 days of exposure to asbestos dust (Nordman and Sorge, 1941). One fortuitous but often cited animal experiment was that of pulmonary asbestosis reported in a dog who served for ten years as a ratter in an asbestos factory. The animal died of alveolar fibrosis and collapse as a result of diffuse distribution of asbestos in the lungs (Schuster, 1931). 

Several human fatalities have resulted from inhalation, dermal contact, or ingestion of ethylene chlorohydrin. Typically, neurotoxic symptoms were described, and death was attributed to cardiac and respiratory collapse. One fatality was caused by exposure to an estimated 300ppm for 2.25 hours. In another fatal case, autopsy showed pulmonary edema and damage to the liver, kidneys, and brain. ... 

Anaphylactic or anaphylactoid reactions may occur following administration of any dose or course of muromonab-CD3. Serious and occasionally life-threatening systemic, cardiovascular, and CNS reactions have been reported. These have included the following Pulmonary edema, especially in patients with volume overload shock cardiovascular collapse cardiac or respiratory arrest seizures coma. Hence, a patient being treated with muromonab-CD3 must be managed in a facility equipped and staffed for cardiopulmonary resuscitation. 

IV administration may result in a rare, severe hypersensitivity reaction marked by a feeling of warmth, pruritus, urticaria, weakness, diaphoresis, nausea, restlessness, tightness in throat, angioedema, cyanosis, pulmonary edema, G1 tract bleeding, and cardiovascular collapse. 

Visual disturbances, faintness, collapse, shock, hypotension, pulmonary edema conjunctival edema. 

Despite the fact that most of the alveolar surface is composited of alveolar epithelium, three primary types of cells are present in the alveoli type I alveolar cells, type II alveolar cells, and alveolar macrophages. Type I alveolar cells are also referred to as squamous pulmonary epithelial cells and are the continuous lining of the alveolar sac. Type II alveolar cells are also referred to as septal cells. Type II alveolar cells secrete the alveolar fluid that is necessary to keep the surface moist and to maintain surface tension of the alveolar fluid surface tension is necessary to keep the alveoli from collapsing. Alveolar fluid is a suitable environment for proteins when compared to the low pH and high protease levels associated with the intestine... 

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