Christen C. Rattenborg

THE EFFECTS OF HEMORRHAGE ON PULMONARY CIRCULATION AND RESPIRATORY GAS EXCHANGE

A close relationship between pulmonary ventilation and blood flow exists in the normal functioning of the lungs. Thus, primary alterations in one of these processes are difficult to distinguish from secondary changes in the other. In order to study these two functions in the intact animal, we have separated them by utilizing a technique which allows us to induce alterations in pulmonary blood flow while keeping ventilation constant in rate and tidal volume. This report describes changes observed in the pulmonary circulation and respiratory gas exchange of dogs in whom blood flow was decreased by hemorrhage and then restored by blood replacement. Studies on experimental animals and human subjects have indicated that all pulmonary vessels are not open at the same time (1), and that the pulmonary circulation is able to accommodate a marked increase in blood flow with little rise in the pulmonary arterial blood pressure (2-7). An increase in blood flow, then, must be accompanied by a decrease in vascular resistance, presumably due to expansion of the pulmonary bed. However, the mechanisms by which such accommodation occurs have not been fully elucidated, and questions remain as to the relative importance of physical forces, the effectiveness of vasomotor control and the significance of local pressor and chemo-reflexes. Moreover, only fragmentary data are available regarding the effects of primary reduction in the pulmonary blood flow, as

Asphyxial Death The Roles of Acute Anoxia, Hypercarbia and Acidosis

&NA; Respiratory and circulatory responses to acute, severe hypoxia, hypoxia combined with moderate hypercarbia, and severe hypercarbia were measured in 22 dogs under conditions of apnea and spontaneous breathing. Survival times before circulatory collapse and physiological death indicated that depletion of oxygen stores progresses ten times more rapidly than accumulation of lethal quantities of hydrogen ion. Consequently, the responses to acute asphyxia differed little from those to breathing an oxygen‐free atmosphere. Depletion of oxygen arrested respiratory drive before causing cardiac arrest in systole. During CO2 retention, acidosis progressively paralyzed the myocardium; respiratory drive persisted until the circulation failed. Arterial Po2 at the time of death was 5 to 10 mm. of mercury during anoxia with and without moderate CO2 retention. Death occurred during extreme CO2 retention over a narrow range of pH of arterial blood, from 6.50 to 6.45, whereas Paco2 varied from 149 to 400 mm. of mercury, suggesting that acidosis causes death, rather than hypercarbia. Hypoxia and acidosis became additive in producing circulatory collapse at a Pao2 below 25 mm. of mercury and at a pHa below 6.80. The rate of depletion of oxygen or accumulation of hydrogen ion did not alter the lethal values of either.

Prolonged oro- or nasotracheal intubation.

From July 1975 to September 1979, 6 patients were treated with truly prolonged endotracheal intubation; the duration ranged from 55–155 days. Only patients who survived after extubation and were discharged from the hospital were included in this study. Of the 6 patients, 4 were still alive as of Nov

Opening and Closing Mechanisms of the Larynx

Opening and closing of the larynx are determined by the intrinsic and extrinsic muscles acting on the elastic forces in the tongue, pharynx, larynx, and trachea. The pharynx is opened or closed by two mechanisms: (1) Contractions of the cricothyroid and of the intrinsic muscles of the larynx open and close the vocal cords. (2) The false cords, ventricle, and true cords accordion open or close in a bellows mechanism. We conclude that the posterior cricoarytenoid opens the laryngeal airway. The cricothyroid together with the posterior cricoarytenoid accentuates this opening. The larynx is also opened by the geniohyoid, mylohyoid, sternothyroid, and middle constrictor. The thyrohyoid, cricothyroid, sternohyoid, and inferior constrictor close the laryngeal airway. Abnormalities in the soft tissues of the neck or of the innervation of the larynx, pharynx, and neck muscles may severely interfere with patency of the laryngeal airway. This occurs in such conditions as vocal cord paralysis, sleep apnea, multiple sclerosis, amyotrophic lateral sclerosis, spastic dysphonia, mandibular fractures or hypodevelopment, and cerebrovascular disease.

Ventilator Surveillance — Routine Application and Quality Control

A ventilator surveillance system has been designed to allow better monitoring of the care of ventilator patients outside intensive care areas. The main reasons for administration of artificial ventilation outside intensive care units have been the fear of superinfection in lymphoma patients, the prolonged artificial ventilation needed for some in neurosurgical patients, and the problem acute overload of intensive care areas.