Biomedical subjects
J L Berk
Publications and source records attributed to J L Berk.
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Profound reflex bradycardia produced by transient hypoxia or hypercapnia in man.
A quadraplegic patient was able to breathe adequately for the first 3 days after his cervical spinal cord was transected by a bullet. However, for several days thereafter spontaneous ventilation became inadequate, most likely due to edema of the cord, and mechanical ventilation was required. When the ventilator was disconnected for required tracheal aspiration, before there was any tracheal stimulation, profound bradycardia, hypotension and syncope occurred within a few seconds. The bradycardia could be diminished by atropine and its onset delayed by prior ventilation with oxygen. Because of the rapid onset of the hemodynamic changes and their correlation with relatively small changes in PaO2 and PaCO2, it is suggested that this vagally mediated bradycardia represents the primary cardiac reflex response to peripheral chemoreceptor stimulation, which, although extensively studied in experimental animals, has not before been described in man. Just as in animals, it seems likely that the inability to hyperventilate permitted the primary cardiac reflex to occur rather than the usual response of tachycardia to chemoreceptor stimulation which is prepotent with spontaneous ventilation. An understanding of this reflex was important in the clinical mangement of this patient.
The role of adrenergic stimulation in the pathogenesis of pulmonary insufficiency.
Recent studies have shown that epinephrine (E), norepinephrine (NE), and isoproterenol (I) caus'e substantial pulmonary shunting. This study was undertaken to determine the role of alpha (pulmonary vasconconstriction) and beta (pulmonary vasodilatation) adrenergic stimulation in the pathogenesis of pulmonary insufficiency. Forty-three mechanically ventilated, anesthetized dogs received infusions of E, alpha and beta stimulant; NE, a relatively pure alpha stimulant; I, a relatively pure beta stimulant; and dextran (D), a drug with no known adrenergic activity. The cardiac output and shunt measurements were determined simultaneously in the control period and four times during a 1 hour infusion. The quadratic equation of best fit was determined for each group for the relationship between the cardiac output and the shunt over a wide range of cardiac outputs, and statistical comparisons were made between all groups of the shunt at the same cardiac output. In all groups an increase in cardiac output was associated with an increase in the shunt, but the magnitude of the increase in the shunt differed significantly with each drug over the entire range, being smallest with D and becoming progressively larger with I, E, and NE, respectively. It is concluded that an increase in the pulmonary blood flow causes an increase in the pulmonary shunt, but that the magnitude of the increase is dependent on the specific pulmonary microcirculatory effects of each drug.
Pulmonary insufficiency produced by norepinephrine: a comparison with epinephrine.
An intravenous infusion of norepinephrine, 2 microgram/kg/min, for 5 hr in anesthetized, mechanically ventilated dogs produced a statistically significant increase in the pulmonary shunt, the cardiac output, and the mean pulmonary artery pressure, but no significant change in the pulmonary wedge pressure and the pulmonary vascular resistance except at 5 min. These hemodynamic changes are qualitatively similar to those produced by the same dose of epinephrine infused for the same time period. However, there were differences in the magnitude of the hemodynamic changes between norepinephrine and epinephrine, as might on the basis of their different pulmonary pharmacologic effects, but the changes were not statistically significant at all times, and more studies are necessary to determine if the differences are real. These studies add support to the thesis that adrenergic stimulation plays an important role in the pathogenesis of the pulmonary insufficiency associated with shock.
Nonocclusive mesenteric vascular insufficiency.
A 74-year-old man had probable nonocclusive intestinal ischemia after myocardial infarction. Angiography and careful monitoring of the patient's hemodynamic status allowed diagnosis and appropriate supportive treatment leading to recovery.
Effect of alpha and beta adrenergic blockade on epinephrine induced pulmonary insufficiency.
Recent studies demonstrated that epinephrine causes significant pulmonary A-V shunting. This study reports the effect of alpha and beta adrenergic blockade on this shunting. Sixty-three anesthetized mongrel dogs were ventilated with a mechanical respirator. Measurements of (1) the pulmonary shunt, (2) cardiac output, (3) mean pulmonary artery, pulmonary capillary wedge and systemic pressures, and (4) pulmonary and systemic vascular resistances were obtained at 5, 15 and 30 minute intervals during the first hour and hourly for 5 hours. Fifteen dogs received no treatment. All others received epinephrine hydrochloride, 2 mug/kg/min for 5 hours. Ten received epinephrine only. Ten were pretreated with propranolol hydrochloride, 250 mug/kg, 12 with phenoxybenzamine, 1 mg/kg, and 16 with phenoxybenzamine and propranolol. Propranolol significantly decreased the epinephrine induced pulmonary shunt at all times and was the most effective drug. Phenoxybenzamine decreased the early shunting, but less than propranolol, and did not decrease the late shunting. Blockade with propranolol and phenoxybenzamine was less effective than propranolol alone. Based on the observed hemodynamic changes it was suggested that beta blockade is effective in reducing epinephrine induced pulmonary insufficiency by favorably altering the flow and distribution of pulmonary blood flow which in turn decreases epinephrine induced ventilation-perfusion inequalities and capillary hypertension both of which result in shunting. Conversely phenoxybenzamine has an unfavorable effect on the pulmonary flow. These studies support previous work in animals and man which showed that beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. Because the amounts of epinephrine used produce blood levels observed in critical illness, these studies add support to a relationship between the increased catecholamine stimulation of critical illness and the associated and often unexplained pulmonary insufficiency.
Gunshot wounds of the esophagus.
During a 4 year period between 1970 and 1974 there were eleven esophageal gunshot wounds representing 52 per cent of the total esophageal perforations. The increased incidence of esophageal gunshot wounds reflects the higher rate of civilian gunshot injuries. There were six perforations in the cervical portion of the esophagus and five in the thoracic portion, with three located above the aortic arch, one in the midesophagus, and one in the lower third. Symptoms are less diagnostic than in esophageal perforations from other causes because the gunshot wound tends to mask the complaints related to mediastinitis. The signs are similar. In 9 patients free air was present in the neck or mediastinum and in 10 patients the diagnosis was confirmed by barium swallow. Of the 2 patients without free air, one had a lateral thoracic wound and esophageal injury was not suspected; the diagnosis was made by drainage of oral feeding through a thoracostomy and confirmed by barium swallow. In the other patient the perforation was found during surgery for hemothorax. Primary repair with drainage was done in the group with cervical injuries. All survived with no serious complications. In the group with thoracic injuries, fistulas developed in 2 of 3 patients who had primary repair with drainage. Two patients with extensive injuries of the esophagus treated by defunctionalization did well but required a second procedure. It is concluded that gunshot wounds of the cervical esophagus, if treated promptly by suture and drainage, will do well. Thoracic injuries represent a more difficult problem and it is suggested that defunctionalization of the esophagus is the safest procedure, particularly if damage is extensive.
Pulmonary insufficiency produced by isoproterenol.
Twelve healthy, anesthetized, mechanically ventilated dogs received an infusion of isoproterenol hydrochloride, 0.1 microgram per kilogram for two hours. There was a rapid and statistically significant increase in the pulmonary shunt, cardiac output and mean pulmonary artery pressure; a significant decrease in the pulmonary vascular resistance, and no significant change in the pulmonary artery wedge pressure. These findings support those of previous studies which demonstrated the beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. The shunt results from ventilation-perfusion inequalities produced by the increased pulmonary blood flow and pulmonary vasodilatation. Because of the production of pulmonary insufficiency, isoproterenol or other beta adrenergic agonists should be used with caution in the critically ill, who often have or may develop the respiratory distress syndrome.
Momitoring the patient in shock: what, when, and how.
In critically ill patients there is frequently more than one problem, which may not be obvious, contributing to the shock state. The history, physical exam, and monitoring devices may not be reliable individually, but must be considered together and interpreted in the light of the pathophysiologic mechanisms involved. A plan for monitoring and treating critically ill patients is outlined. The advantages and limitations of various monitoring techniques are discussed.
Use of vasoactive drugs in the treatment of shock.
The effective use of vasoactive drugs in shock requires an understanding of the pathophysiologic mechanisms involved in the various types and stages of shock and knowledge of the specific pharmacologic effects of each drug in the abnormal state. Vasoactive drugs should be used after the primary and secondary causes of shock have been corrected. Specific vasoactive drugs should be selected on the basis of measured hemodynamic abnormalities.
Pulmonary anatomic arteriovenous shunting caused by epinephrine.
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Pulmonary insufficiency caused by epinephrine.
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The treatment of shock with beta adrenergic blockade.
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The dumping syndrome.
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The hypoglycemic effect of propranolol.
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The role of beta adrenergic blockade in the treatment of septic shock.
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