Evaluation of the cardiovascular system during various circulatory stresses Progress report, 1 Jun. 1969 - 30 May 1970
Cardiovascular system evaluation during various circulatory stresses
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Cardiovascular system evaluation during various circulatory stresses
The data collected from a Space Shuttle crew to investigate cardiovascular changes due to microgravity are presented. The experimental procedures which involved preflight, immediate postflight, and one week following postflight echocardiograms of 13 individuals are described. The immediate postflight results reveal a 20 percent decrease in stroke volume, a 16 percent decrease in left ventricular diastolic volume index (LVDVI), no change in systolic volume, blood pressure, or cardiac index, and a 24 percent increase in heart rate. One week later a 17 percent stroke volume increase, a 29 percent increase in cardiac index, and normal blood pressure, and LVDVI were observed. It is concluded that upon reexposure to gravity a readaptation process for the cardiovascular system occurs.
Principles and descriptive fragments which may contribute to a model of the regulating chains in the cardiovascular system are presented. Attention is given to the strain sensitivity of blood vessels, the law of the autonomy of the heart beat oscillator, the law of the encapsulation of body fluids, the law of the conservation of protein, the law of minimum 'arterial' pressure, the design of the 'mammalian' kidney, questions of homeokinetic organization, and the development of self-regulatory chains. Details concerning the development program for the heart muscle are considered along with the speed of response of the breathing rate and the significance of the pulmonary vascular pressure-flow characteristics.
Mathematical models used to study complex physiological control systems are discussed. Efforts were made to modify a model of the cardiovascular system for use in studying lower body negative pressure. A computer program was written which allows orderly, straightforward expansion to include exercise, metabolism (thermal stress), respiration, and other body functions.
The present work discusses a model of the cardiovascular system and related subsystems capable of long-term simulations of the type desired for in-space hypogravic human physiological performance prediction. The discussion centers around the model of Guyton and modifications of it. In order to draw attention to the fluid handling capabilities of the model, one of several transfusion simulations performed is presented, namely, the isotonic saline transfusion simulation.
This paper reports on a theoretical investigation into the effects of vasomotion on blood through the human cardiovascular system. The finite element method has been used to analyse the model. Vasoconstriction and vasodilation may be effected either through the action of the central nervous system or autoregulation. One of the conditions responsible for vasomotion is exercise. The proposed model has been solved and quantitative results of flows and pressures due to changing the conductances of specific networks of arterioles, capillaries and venules comprising the arms, legs, stomach and their combinations have been obtained.
Electronic circuit processes arterial blood pressure waveform to produce discrete signals that coincide with beginning and end of left ventricular ejection. Output signals provide timing signals for computers that monitor cardiovascular systems. Circuit operates reliably for heart rates between 50 and 200 beats per minute.
Bed rest is a well-accepted analog of space flight that has been used extensively to investigate physiological adaptations in a larger number of subjects in a shorter amount of time than can be studied with space flight and without the confounding effects associated with normal mission operations. However, comparison across studies of different bed rest durations, between sexes, and between various countermeasure protocols have been hampered by dissimilarities in bed rest conditions, measurement protocols, and testing schedules. To address these concerns, NASA instituted standard bed rest conditions and standard measures for all physiological disciplines participating in studies conducted at the Flight Analogs Research Unit (FARU) at the University of Texas-Medical Branch. Investigators for individual studies employed their own targeted study protocols to address specific hypothesis-driven questions, but standard measures tests were conducted within these studies on a non-interference basis to maximize data availability while reducing the need to implement multiple bed rest studies to understand the effects of a specific countermeasure. When possible, bed rest standard measures protocols were similar to tests nominally used for medically-required measures or research protocols conducted before and after Space Shuttle and International Space Station missions. Specifically, bed rest standard measures for the cardiovascular system implemented before, during, and after bed rest at the FARU included plasma volume (carbon monoxide rebreathing), cardiac mass and function (2D, 3D and Doppler echocardiography), and orthostatic tolerance testing (15- or 30-minutes of 80 degree head-up tilt). Results to-date indicate that when countermeasures are not employed, plasma volume decreases and the incidence of presyncope during head-up tilt is more frequent even after short-duration bed rest while reductions in cardiac function and mass are progressive as bed rest duration increases. Additionally, while plasma volume loss can be corrected and cardiac mass can be prevented with properly applied countermeasures, orthostatic tolerance is more difficult to protect when supine exercise is the only countermeasure. Similar results have been observed after space flight. Plasma volume, cardiac chamber volume, and orthostatic tolerance recover relatively quickly with resumption of ambulation and normal activity levels after bed rest but restoration of cardiac mass is prolonged.
Mathematical model for cardiovascular regulation during weightlessness
Ground-based simulation studies have been conducted to clarify the problems of the cardiovascular adaptation to alterations in gravitational force. Simulated microgravity experiments resulted in increases in cardiac stretch, urine flow, and sodium excretion, which were accompanied by lower plasma renin, aldosterone, and ADH. There appears to be a decrease in plasma volume as well as in sympathetic tone after 2-3 days of 0 Gz. Complete adjustment to 0 Gz is found within 8 h without a decrease in plasma volume, when subjects are allowed to dehydrate mildly.
During the acute transition from lying supine to standing upright, a large volume of blood suddenly moves from the chest into the legs. To prevent fainting, the blood pressure control system senses this change immediately, and rapidly adjusts flow (by increasing heart rate) and resistance to flow (by constricting the blood vessels) to restore blood pressure and maintain brain blood flow. If this system is inadequate, the brain has a backup plan. Blood vessels in the brain can adjust their diameter to keep blood flow constant. If blood pressure drops, the brain blood vessels dilate; if blood pressure increases, the brain blood vessels constrict. This process, which is called autoregulation, allows the brain to maintain a steady stream of oxygen, even when blood pressure changes. We examined what changes in the blood pressure control system or cerebral autoregulation contribute to the blood pressure control problems seen after spaceflight. We asked: (1) does the adaptation to spaceflight cause an adaptation in the blood pressure control system that impairs the ability of the system to constrict blood vessels on return to Earth?; (2) if such a defect exists, could we pinpoint the neural pathways involved?; and (3) does cerebral autoregulation become abnormal during spaceflight, impairing the body s ability to maintain constant brain blood flow when standing upright on Earth? We stressed the blood pressure control system using lower body negative pressure, upright tilt, handgrip exercise, and cold stimulation of the hand. Standard cardiovascular parameters were measured along with sympathetic nerve activity (the nerve activity causing blood vessels to constrict) and brain blood flow. We confirmed that the primary cardiovascular effect of spaceflight was a postflight reduction in upright stroke volume (the amount of blood the heart pumps per beat). Heart rate increased appropriately for the reduction in stroke volume, thereby showing that changes in heart rate regulation alone cannot be responsible for orthostatic hypotension after spaceflight. All of the astronauts in our study had an increase in sympathetic nerve activity during upright tilting on Earth postflight. This increase was well calibrated for the reduction in stroke volume induced by the upright posture. The results obtained from stimulating the sympathetic nervous system using handgrip exercise or cold stress were also entirely normal during and after spaceflight. No astronaut had reduced cerebral blood flow during upright tilt, and cerebral autoregulation was normal or even enhanced inflight. These experiments show that the cardiovascular adaptation to spaceflight does not lead to a defect in the regulation of blood vessel constriction via sympathetic nerve activity. In addition, cerebral autoregulation is well-maintained. It is possible that despite the increased sympathetic nerve activity, blood vessels did not respond with a greater degree of constriction than occurred preflight, possibly uncovering a limit of vasoconstrictor reserve.
Devices and techniques for measuring and analyzing systolic time intervals and quantitative phonocardiograms were initiated during Apollo 17. The data show that the systolic time interval from Apollo 17 crewmen remained elevated longer postflight than the response criteria of heart rate, blood pressure, and percent change in leg volume all of which had returned to preflight levels by the second day postflight. Although the systolic time interval values were only slightly outside the preflight fiducial limits, this finding suggested that: the analysis of systolic time intervals may help to identify the mechanisms of postflight orthostatic intolerance by virtue of measuring ventricular function more directly and, the noninvasive technique may prove useful in determining the extent and duration of cardiovascular instability after long duration space flight. The systolic time intervals obtained on the Apollo 17 crewmen during lower body negative pressure were similar to those noted in patients with significant heart disease.
Cardiac response to chemotherapy after myocardial infraction and diagnostic methods of heart disease in man and animals
Hardware and techniques for studying human circulatory performance in space environment
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Extensive studies of blood circulation functions during manned space flight demonstrated a pronounced tendency toward an increase in minute volume of the blood and a decrease in pulse wave propagation rate. Individual blood circulation indices had large amplitude fluctuations. Physical work loads caused slow recovery of heart rate, arterial pressure and minute blood volume.
The adequate modeling of physiological reactions inherent to the state of weightlessness has become a matter of particular urgency in space medicine. This modeling is necessary for studying the phenomenology and degree of disorders, prognostication of the crew's health, and developing the various preventive measures employed in space flights. A comparison is made of the physiological effects brought about by bed rest in a horizontal and antiorthostatic body position. A study is done of the influence of brief antiorthostatic hypokinesia, simulating the acute period of adaptation to weightlessness, on circulation and on a number of involved analytical systems. The basic model accepted is antiorthostatic hypokinesia with a body position declination angle of 4 deg (head lower than feet). The experiment's duration is dictated by the objectives of the research.
A species predisposition to hypertensive and ischemic heart disease occurs in mammals only at the level of primates, and is associated with social regulation of biological reactions. The specific physiological mechanism giving rise to psychonerogenic pathology may be an inhibition of the motor component of the agressive-defensive response. Repeated combination of pursuit with subsequent immobilization resulted in four out of five experimental baboons developing serious arterial hypertension and ischemic lesion of the heart which lasted many years.