Circuit for automatically zeroing aortic flow base line from electromagnetic flowmeter

1977 ◽  
Vol 232 (5) ◽  
pp. H534-H536
Author(s):  
D. G. Wantzelius ◽  
K. L. Goetz

We describe an inexpensive circuit designed to correct base-line drift of electromagnetic flowmeters automatically when cardiac output is being measured. The circuit measures the flowmeter output voltage during a portion of each diastole when blood flow in the aorta is assumed to be zero. Any deviation of the flowmeter output voltage from zero during this time represents either base-line offset or drift. The output voltage obtained during zero flow conditions is stored throughout the next cardiac cycle and subtracted continuously from the flowmeter output during each beat, thus giving a beat-by-beat correction of any base-line drift.

1963 ◽  
Vol 18 (6) ◽  
pp. 1265-1267 ◽  
Author(s):  
Allen M. Scher ◽  
Julian Zepeda ◽  
Otis F. Brown

The availability of a stable, highly sensitive commercial recorder led us to construct a simple delay unit and square-wave driver for the purpose of measuring blood flow electromagnetically. The construction of the flowmeter heads is described briefly, and some analysis is made of possible deficiencies in flowmeter heads employing iron cores. The flow-measuring system is sensitive and linear and, when the magnet drive is turned off, the base line is within a few microvolts of true zero flow. blood flow in intact animals; epoxyresin embedding implantation Submitted on March 4, 1963


1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.


1960 ◽  
Vol 15 (6) ◽  
pp. 1062-1064 ◽  
Author(s):  
Edward J. Hershgold ◽  
Sheldon H. Steiner ◽  
Leo A. Sapirstein

The applicability of the hematocrit dilution technique employing arterial blood conductivity changes to the determination of the cardiac output has been extended by a) electronic damping of the detecting circuits, which permits greater amplification of the signal without increasing the variability of the base line that occurs during each cardiac cycle, and by b) development of a solution isoosmolar and isoconductive with plasma that substitutes for autogenous plasma in the procedure. The preparation of the synthetic solution is described. It is shown that this solution gives results indistinguishable from those obtained with plasma. Values are given for the conductivity and osmolarity of dog plasma. Submitted on December 3, 1959


Author(s):  
Dr Mark Harrison

2.1 Control of blood pressure and heart rate, 445 2.2 Control of heart rate, 446 2.3 Cardiac output (CO), 447 2.4 Measurement of cardiac output (CO), 450 2.5 Blood flow peripherally, 451 2.6 The cardiac cycle, 454 2.7 ECG, 458 2.8 Pharmacological manipulation of the heart and peripheral circulation, ...


1985 ◽  
Vol 58 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
S. Gelman ◽  
K. C. Fowler ◽  
S. P. Bishop ◽  
L. R. Smith

Cardiac output distribution and regional blood flow were studied during hypocarbia independent of changes in ventilatory parameters. Fifteen cynomolgus monkeys were anesthetized with methohexital sodium (8 mg/kg im) and hyperventilated through an endotracheal tube. Hypocarbia at two levels, 28 +/- 1.8 and 17 +/- 0.6 Torr, was achieved by a stepwise decreasing CO2 flow into the semiclosed system. Regional blood flow was determined with labeled microspheres. At each stage of experiments two sets of microspheres (9 and 15 microns diam) were used simultaneously. The use of two microsphere sizes allowed evaluation of the relationship between total (nutritive and nonnutritive) tissue blood flow, determined with 15-microns spheres, and nutritive blood flow, determined with 9-microns spheres. There was no change in cardiac output or arterial pressure during both degrees of studied hypocarbia. Hypocarbia was accompanied by a decrease in myocardial blood flow determined with 15-microns spheres and preservation of the flow determined with 9-microns spheres. Splenic blood flow was decreased, whereas hepatic arterial blood flow was increased during both levels of hypocarbia. Blood flow through the brain, renal cortex, and gut showed a biphasic response to hypocarbia: during hypocarbia at 28 +/- 1.8 Torr, blood flow determined with 15-microns spheres was unchanged (in the gut) or decreased (in the brain and kidneys), whereas blood flow determined with 9-microns spheres was decreased. During hypocarbia at 17 +/- 0.6 Torr, blood flow determined with 9-microns spheres had a tendency to restore to base-line values.


Author(s):  
Manish Kalla ◽  
Neil Herring

This chapter discusses normal function of the cardiovascular system, including cardiac physiology (the cardiac cycle, ECG, blood flow and heart sounds, control of cardiac output), vascular physiology (control of local blood flow, capillary transfer), integrated cardiovascular control,


1976 ◽  
Vol 40 (5) ◽  
pp. 849-853 ◽  
Author(s):  
G. M. Walsh ◽  
M. Tsuchiya ◽  
E. D. Frohlich

The direct Fick procedure for cardiac output determination in rat was validated by simultaneous comparison with electromagnetic flowmeter techniques. Significant coefficients of correlation were obtained between absolute cardiac output values (r = 0.789, P less than 0.001), increases (r = 0.768, P less than 0.001) and decreases (r = 0.672, P less than 0.01) in cardiac output detected by the two methods. As demonstrated in other species, cardiac output values of the Fick procedure in the rat were between 40 and 58% greater than respective electromagnetic flow probe values; however, percent changes in cardiac output obtained by the two methods were similar. The larger values of cardiac output obtained by the direct Fick method may be related, to a great extent, to the distribution of blood flow to the coronary and bronchial circulations. Fick cardiac output measurements were reproducible within rats, and the degree of variation in values among rats was similar to that obtained with the flowmeter procedure. The result indicate that the Fick meth od provides a valid estimation of cardiac output in the rat, with the ability to detect moderate changes (22–36%) in cardiac output.


1982 ◽  
Vol 53 (1) ◽  
pp. 110-116 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
L. E. Farhi

We have measured the effects of normobaric hyperoxia on arterial and mixed venous gas tensions, cardiac output, heart rate, right atrial, pulmonary, and aortic pressures in 12 conscious chronically instrumented sheep. Regional blood flow to brain, heart, kidney, intestines, and respiratory muscles was assessed in five sheep by injecting 15-micrometers microspheres labeled with gamma-emitting isotopes. Survival time ranged from 60 to 120 h (mean = 80 h). All variables except arterial O2 partial pressure (PaO2) and mixed venous O2 partial pressure remained at base-line level during the first 40 h of exposure, after which PaO2 decreased gradually but remained above 200 Torr at death. After this there was a progressive uncompensated respiratory acidosis with terminal arterial CO2 partial pressure values exceeding 90 Torr. There was a considerable rise in the brain blood flow, whereas flow to the other organs either remained unchanged or increased in proportion to cardiac output. Our experiments also showed that systemic hyperoxic vasoconstriction did not occur, and any local changes were not of sufficient magnitude to affect perfusion.


1989 ◽  
Vol 256 (6) ◽  
pp. H1651-H1658
Author(s):  
C. L. Rosen ◽  
A. Cote ◽  
G. G. Haddad

To investigate the effects of enkephalins on cardiac output and regional blood flow, we administered D-Ala-D-Leu-enkephalin (DADLE) intracisternally (ic) to 14 chronically instrumented unanesthetized dogs. Measurements were made at base line, 20, 45, and 75 min after DADLE (25 or 125 micrograms/kg) and 15 min after naloxone (5 micrograms/kg ic). After 125 micrograms/kg DADLE, all animals developed hypoventilation, bradycardia, and decreased O2 consumption without hypotension. Cardiac output decreased (-34%), but brain blood flow increased (+110%). Blood flow decreased to the diaphragm (-38%), heart (-21%), skeletal muscle (-40%), skin (-67%), pancreas (-79%), and gastrointestinal tract (-26%). After 25 micrograms/kg DADLE, there were no consistent changes in cardiac output or regional blood flow. Four additional animals (without DADLE) were exposed to altered inspired gases to reproduce the blood gas changes after DADLE. These animals developed hyperventilation without bradycardia and increased brain (+114%) and diaphragm (+649%) blood flow. We conclude that centrally administered enkephalins produce 1) a parallel decrease in ventilation, heart rate, O2 consumption, and cardiac output and 2) a major blood flow redistribution, primarily dictated by the effects of opioids on ventilation, heart rate, and metabolism.


1982 ◽  
Vol 243 (4) ◽  
pp. H560-H565
Author(s):  
F. Charocopos ◽  
P. Hatzinikolaou ◽  
W. G. North ◽  
H. Gavras

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.


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