Biomedical subjects
W A Tweed
Publications and source records attributed to W A Tweed.
Retention of cardiopulmonary resuscitation skills after initial overtraining.
The authors have examined cardiopulmonary resuscitation (CPR) skills retention in a police force initially trained to instructor level performance skills as defined by the 1977 American Heart Association Instructor Manual. In 1977, the entire Winnipeg Police Force received a basic 8-h course of CPR training with recording manikins. Each training session was followed by a written test and a performance test on the recording manikin using instructor level tape criteria as the standard. Between 12 and 18 months later, 116 personnel were randomly selected for retesting. The first min of one-man CPR on the two tapes was compared. Retention was expressed as a percentage, i.e., retest score/training score x 100. Retention scores were as follows: knowledge, 76%; assessment skills, 83%; call for help, 85%; numbers of adequate ventilations, 100%; numbers of adequate compressions, 97%. Total assessment time and incidence of potentially injurious performance were the same. Deliverate overtraining of highly motivated and mature nonmedical basic rescuers results in satisfactory skills retention for at least 1 year.
Regional cerebral blood flow changes during severe fetal asphyxia produced by slow partial umbilical cord compression.
We studied the effects of severe partial asphyxia on regional cerebral blood flow and arterial blood pressure in the unanesthetized, physiologically stable fetal lamb. Cerebral blood flow was measured by the microsphere technique before and during partial umbilical cord compression. Asphyxia sufficient to decrease pH from 7.40 to 7.04 and reduce oxygen saturation from 50% to 19% increased cerebral blood flow to all areas of the brain with the largest increases going to the brain stem (275% of control) and deep cerebral structures (240% of control). Fetal arterial blood pressures increased from a mean of 58 mm Hg to a mean of 71 mm. Hg during asphyxia. The blood pressure increases correlated closely with the regional cerebral blood flow increases. There was a poor correlation between cerebral blood flow increases and changes in Paco2' pH, or oxygen saturation. We conclude that during severe fetal asphyxia arterial blood pressure is the critical factor in determining cerebral blood flow.
Tissue albumin and water content in the early stages of vasogenic brain edema formation.
Brain edema (BE) research lacks quantitative regional methods. We modified the method of Pappius and McCann (1969), who used radioactive iodinated I125 serum albumin (RISA) as a label for vasogenic BE fluid. To correct for intravascular plasma volume we used Cr51 labelled red blood cells and calculated equivalent extravascular plasma volume (EVPV). The modified RISA method was compared with a standard method for measuring increased tissue water, i.e. the change in wet:dry weights. Anesthetized rabbits were subjected to unilateral cortical freeze injury and sacrificed three hours later. The lesion corresponding to the area of blood brain barrier (BBB) breakdown was delineated by Evan's blue staining. That area and the two adjacent poles were sectioned. The contralateral hemisphere was used as the control. Good agreement was found between the two methods. By the modified RISA method, 4.08% of the wet weight of the injured hemisphere was EVPV while the decrease in dry weight corresponded to 5.56% edema. In the freeze lesion, however, where BBB breakdown occurred extravascular (EV) protein exceeded EV water, while adjacent to the lesion in the area with intact BBB, EV water exceeded EV protein. This suggests that the diffusion rate for water through brain tissue exceeds that of albumin in the early stages of vasogenic BE formation. We conclude that the modified RISA method is a satisfactory measure of regional vasogenic BE in acute animal experiments.
Pressure passive cerebral blood flow and breakdown of the blood-brain barrier in experimental fetal asphyxia.
Cerebral blood flow (CBF) was studied in non-exteriorized near-term sheep fetuses using the radioactive microsphere technique. By partially occluding the umbilical vessels for a period of 1--1 1/2 hours a progressive and severe asphyxia with a final arterial pH of 6.90 was achieved. Varying the mean arterial blood pressure in the fetuses by blood withdrawal or infusion in this state, CBF was measured at different perfusion pressures (mean arterial blood pressure (MABP) minus central venous pressure (CVP)). A passive flow/pressure relationship--loss of autoregulation--was found, with hyperemia reaching CBF values up to 6 times normal at normal MABP of about 60 to 70 mmHg, and severe ischemia reaching CBF values close to zero in large cortical areas at MABP of 30 mmHg. CVP remained essentially unchanged at 10--15 mmHg. The severe and prolonged asphyxia rendered the blood-brain barrier leaky to the albumin tracer Evans blue. In four other fetuses umbilical cord clamping was omitted. However, only in one of these cases was acidosis completely avoided, and CBF autoregulation maintained. The three other fetuses were acidotic at the end of the surgical procedure and had impaired autoregulation.
Heart-Alert: emergency resuscitation training in the community.
One approach to reducing avoidable mortality from coronary artery disease is to provide resuscitation capability in the community. In Manitoba this is the function of the Heart-Alert program, sponsored by the Manitoba Heart Foundation. The program is based on public and professional education dealing with the recognition and immediate care of cardiac emergencies, including cardiopulmonary resuscitation (CPR). The three components to the program are (a) training in basic CPR for all health care and community rescue groups; (b) training in definitive CPR for physicians, critical care nurses and advanced emergency medical technicians; and (c) education of the public to recognize the signs of impending or actual cardiac emergencies and to take appropriate action to summon quickly an emergency rescue team.The initial emphasis of the program has been on developing an organizational structure and a training network for basic CPR. A corps of instructor-trainers and instructors has been certified to implement CPR training in the medical and community target groups. Developmental problems include problems of quality control, of providing for self-sustaining and continued expansion, and of evaluation of the overall results.It is suggested that widespread implementation of CPR training is facilitated by the incorporation of CPR into existing training activities, particularly those of the medical, nursing and other health care disciplines, those of community protection agencies such as police, fire and ambulance departments, and those of volunteer groups concerned with rescue work and first-aid. If the impetus, organizational structure and instructor training are provided by a strategic agency, wide dissemination of CPR training is then possible at relatively modest cost.
Resuscitation from cardiopulmonary arrest during accidental hypothermia due to exhaustion and exposure.
A 16-year-old boy with accidental hypothermia and cardiopulmonary arrest due to exhaustion and exposure was resuscitated after warming measures -- hot wet towels, hot water bottles, and hot water enemas and gastric lavage -- had increased his rectal temperature from 25.2 to 28.0 degrees C. Despite prolonged cardiopulmonary arrest, recovery was almost complete, with no evident cerebral damage. Cardiopulmonary resuscitation procedures should not be abandoned until the body temperature is more than 30 degrees C, because the prognosis in cases of accidental hypothermia without associated disease is excellent if cardiac function can be re-established.
Breakdown of blood/brain barrier in kernicterus.
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Serial changes in cerebral blood flow and metabolism following cerebral anoxia in man.
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Causes of the low flow state following total cerebral ischemia.
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Mechanisms of the "low-flow" state during resuscitation of the totally ischemic brain.
Resuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a postischemic "low-flow"state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked imporvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central arotic pressure and cerebral perfusion pressure. Hyperkalemic induced vasoconstriction has also been postulated as a cause of the "low-flow/. We have, therefore, investigated the in vitro effects of increasing potassium ion concentration on cerebrovascular smooth muscle strips. Large arteries constrict, while small arteries dilate in response to hyperkalemia. The net effect on cerebral blood flow remains unsettled. Our research to date suggests that resuscitation of the totally ischemic brain, in animal models at least, is enhanced by epinephrine, mainly via its effects on central aortic pressure.
Cerebral blood flow in patients with intracranial pressure elevation due to traumatic brain edema.
The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pronounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.
Cerebral circulation after head injury. Part 2: The effects of traumatic brain edema.
The authors have assessed the effects of subacute traumatic brain edema (BE) on cerebral circulation and metabolism, and on clinical outcome. Fifty-five severely injured, comatose, young patients who survived for more than 24 hours were studied on 78 occasions within 30 days of injury. After hematomas had been surgically evacuated, BE was diagnosed by radiological evidence of brain swelling, demonstrated by cerebral angiograms and ventriculograms. At identical levels of carbon dioxide pressure, intracranial pressure was significantly elevated in the Edema Group to twice the value in the No Edema Group (27.1 vs 14.1 torr). There were, however, no significant differences in cerebral perfusion pressure cerebral blood flow, resistance to blood flow, cerebral metabolic oxygen rate, ventricular cerebrospinal fluid acid-base, lactate, K+ or Na+ concentrations, or in clinical outcome. It is concluded that this type of subacute traumatic BE, which is significantly associated with surgical lesions, is not of major hemodynamic or clinical significance in intensively treated patients, and does not cause cerebral ischemia. Patient outcome is determined more by the severity of the initial diffuse cortical and subcortical injury than by the presence or absence of subacute BE.
Cerebrospinal-fluid acid-base and electrolyte changes resulting from cerebral anoxia in man.
To study metabolic changes in the central nervous system after profound anoxia, we measured changes in cisternal and lumbar cerebrospinal fluid. Acid-base values and electrolyte concentrations were determined in cisternal and lumbar fluid from 12 severely anoxic patients (cardiac arrest), and from 15 within 24 hours after cardiac resuscitation. In the severely anoxia patients the normal cisternal-lumbar pH gradient was reversed, cisternal fluid was more acid (pH 6.815 vs. 6.953), and cisternal potassium concentration was twice that of lumbar (6.7 vs 3.5 mEq per liter). These findings indicate that during anoxia potassium and hydrogen ion flow from brain cells into the brain extracellular fluid, and that acute changes are reflected more accurately by cisternal than by lumbar fluid. In resuscitated patients cisternal fluid was normal, and normal cisternal-lumbar differences were found; thus, the normal milieu of brain cells is rapidly reestablished after resuscitation.
rCBF in impending brain death.
Regional cerebral blood flow (rCBF) was measured in three patients after relief of elevated intracranial pressure and restoration of normal cerebral perfusion pressure. Two patients, studied within 4 hours after closed head injury were found to have marked impairment of cortical blood flow and elevation of cerebrovascular resistance. We suggest that this picture is indicative of impending brain death, and may be the result of a long period of severe cerebral ischemia. The third patient, who had a shorter period of intracranial hypertension occurring during anaesthetic induction, responded to reduction of ICP quite differently with a transient relative hyperaemia. The physiopathological explanations for these two different types of flow response and their possible clinical significance are discussed.
Myocardial force-velocity relations during ketamine anesthesia at constant heart rate.
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Cerebral circulation after head injury. 1. Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations.
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Prognosis after head injury based on early clinical examination.
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