Cardiac output, coronary blood flow, and blood gases during open-chest standard and compression-active-decompression cardiopulmonary resuscitation

Resuscitation ◽  
2002 ◽  
Vol 55 (3) ◽  
pp. 309-316 ◽  
Author(s):  
Milo Engoren ◽  
Fred Severyn ◽  
Nancy Fenn-Buderer ◽  
Michael DeFrank
1989 ◽  
Vol 17 (8) ◽  
pp. 768-771 ◽  
Author(s):  
SHLOMO A. BEN-HAIM ◽  
RONA SHOFTI ◽  
BILL OSTROW ◽  
URI DINNAR

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P < .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.


1982 ◽  
Vol 242 (5) ◽  
pp. R434-R440
Author(s):  
T. McKean

Beavers (Castor canadensis) and nutria (Myocastor coypus) were anesthetized with halothane and catheters placed in the left ventricle, aorta and pulmonary artery, right ventricle or right atrium. The animals were strapped to a board and following recovery from anesthesia the following measurements were taken: regional distribution of blood flow, cardiac output, O2 consumption, arterial and venous blood gases, and pH. The animal was then immersed in 15-20 degrees C water for up to 2.75 min (nutria) or 4 min (beaver) and the measurements repeated. Heart rate and cardiac output decreased by 80 and 75%, respectively. Arterial and venous oxygen partial pressure and content fell as did pH whereas CO2 pressures rose during diving. Oxygen consumption at rest was 124 and 102% of that predicted on the basis of body mass for the beaver and nutria, respectively. Rate of decline of O2 stores during diving decreased by 93% in beavers and 89% in nutria compared to the predive value. Regional blood flow decreased to all organs except the adrenals, heart, and lungs. Blood flow to the brain increased during diving.


1959 ◽  
Vol 196 (2) ◽  
pp. 391-393 ◽  
Author(s):  
Richard L. Farrand ◽  
Steven M. Horvath

Khellin, a drug employed as a coronary dilator, was tested to determine its effects on the cardiovascular system of the dog. Ten mongrel dogs were anesthetized with Nembutal and, after control observations were made, given an intravenous administration of 1 mg/kg body weight of khellin. Coronary blood flow and cardiac output samples were drawn during the control period and at 10, 40 and 80 minutes after administration of the drug Cardiac output was calculated by the direct Fick principle and coronary blood flow by the nitrous oxide method. There was a significant (5%) increase in the arterial oxygen content during the 10- and 40-minute intervals, but no change was observed at 80 minutes. An increase in arterial-mixed venous oxygen difference occurred at 40 and 80 minutes. No change in systemic arterial pressure or cardiac output was noted at any time. Coronary blood flow had decreased slightly at 80 minutes. A significant decrease in carbon dioxide content of the arterial, pulmonary arterial and coronary sinus blood was observed, possibly as a consequence of hyperventilation. Khellin appeared to alter the metabolism of the myocardial and splanchnic tissues.


1959 ◽  
Vol 261 (13) ◽  
pp. 653-655 ◽  
Author(s):  
George G. Rowe ◽  
George M. Maxwell ◽  
Cesar A. Castillo ◽  
C. W. Crumpton ◽  
Richard J. Botham ◽  
...  

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.


1993 ◽  
Vol 74 (4) ◽  
pp. 1672-1678 ◽  
Author(s):  
D. D. Malcolm ◽  
J. L. Segar ◽  
J. E. Robillard ◽  
S. Chemtob

We examined whether prostanoids contribute to the impaired cardiac function and decrease in regional blood flow induced by increasing mean airway pressure. Using microspheres, we measured cardiac output and major organ blood flow and assayed prostaglandin E2, 6-ketoprostaglandin F1 alpha, and thromboxane B2 in blood at mean airway pressures of 5–25 cmH2O in mechanically ventilated newborn piglets treated with ibuprofen (40 mg/kg, n = 6), indomethacin (0.3 mg/kg, n = 6), or vehicle (n = 6). Blood gases and pH were stable throughout the experiments. Prostanoid levels remained constant with increasing mean airway pressure in vehicle-treated pigs and were unchanged by indomethacin. However, ibuprofen decreased the prostanoid levels at all mean airway pressures studied (P < 0.01). As ventilatory pressure was progressively increased, cardiac output decreased gradually and similarly by 42–45% (P < 0.05) in all groups. At the highest mean airway pressure, blood flow decreased to the kidneys by 37–57%, to the ileum by 58–74%, and to the colon by 53–71% (P < 0.05) in all groups. Cerebral blood flow remained constant at all ventilatory pressures regardless of the treatment. There was no difference in cardiac output and regional hemodynamics between ibuprofen- and vehicle-treated animals. However, after indomethacin, ileal blood flow at the higher ventilatory pressures was 41–46% lower and cerebral blood flow at all mean airway pressures was 14–25% lower than after the other treatments (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


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