Continuous Airway Pressure Breathing With the Head-Box in the Newborn Lamb: Effects on Regional Blood Flows

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Airway Pressure ◽  
Left Ventricular Pressure ◽  
Blood Gases ◽  
Ocular Blood Flow ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Blood Flows ◽  
Arterial Blood

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.

Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Arterial Blood ◽  
Time Flow ◽  
The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

Indomethacin compromises hemodynamics during positive-pressure ventilation, independently of prostanoids

1993 ◽  
Vol 74 (4) ◽  
pp. 1672-1678 ◽  
Author(s):  
D. D. Malcolm ◽  
J. L. Segar ◽  
J. E. Robillard ◽  
S. Chemtob
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Airway Pressure ◽  
Regional Blood Flow ◽  
Blood Gases ◽  
Positive Pressure ◽  
Organ Blood Flow ◽  
Mean Airway Pressure ◽  
Airway Pressures

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)

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Hypopnea consequent to reduced pulmonary blood flow in the dog

1979 ◽  
Vol 46 (6) ◽  
pp. 1171-1177 ◽  
Author(s):  
R. W. Stremel ◽  
B. J. Whipp ◽  
R. Casaburi ◽  
D. J. Huntsman ◽  
K. Wasserman
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Blood Gases ◽  
Left Ventricular ◽  
Intact Group ◽  
Average Decrease ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

The ventilatory responses to diminished pulmonary blood flow (Qc), as a result of partial cardiopulmonary bypass (PCB), were studied in chloralose-urethan-anesthetized dogs. Qc was reduced by diverting vena caval blood through a membrane gas exchanger and returning it to the ascending aorta. PCB flows of 400--1,600 ml/min were utilized for durations of 2--3 min. Decreasing Qc, while maintaining systemic arterial blood gases and perfusion, results in a significant (P less than 0.05) decrease in expiratory ventilation (VE) (15.9%) and alveolar ventilation (VA) (31.0%). The ventilatory decreases demonstrated for this intact group persist after bilateral cervical vagotomy (Vx), carotid body and carotid sinus denervation (Cx), and combined Vx and Cx. The changes in VE and VA were significantly (P less than 0.001) correlated with VCO2 changes, r = 0.80 and r = 0.93, respectively. These ventilatory changes were associated with an overall average decrease in left ventricular PCO2 of 2.1 Torr; this decrease was significant (P less than 0.05) only in the intact and Cx groups. Decreasing pulmonary blood flow results in a decrease in ventilation that may be CO2 related; however, the exact mechanism remains obscure but must have a component that is independent of vagally mediated cardiac and pulmonary afferents and peripheral baroreceptor and chemoreceptor afferents.

Effects of acute hypercapnia on the central and peripheral circulation of conscious sheep

1983 ◽  
Vol 54 (3) ◽  
pp. 803-808 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
J. A. Krasney ◽  
L. E. Farhi
Keyword(s):  
Minute Ventilation ◽  
Respiratory Muscles ◽  
Blood Gases ◽  
Peripheral Circulation ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Co2 Partial Pressure ◽  
Blood Flows ◽  
Arterial Blood ◽  
Conscious Sheep

We studied the cardiorespiratory effects of acute hypercapnia in 10 unanesthetized sheep. After a 15-min exposure to either 7.3 or 10% CO2 in air, we measured arterial blood gases, minute ventilation (VE), O2 consumption (VO2), cardiac output (Q), heart rate (HR), an index of left ventricular contractility [(dP/dt)/P], and vascular pressures. In addition, regional flows to all major organs were determined by injecting 15-microns radiolabeled microspheres into the left heart. Exposure to 7.3% CO2 (arterial CO2 partial pressure, PaCO2, 58 Torr) resulted in increased VE, (dP/dt)/P, and higher blood flows to the brain and respiratory muscles. All other variables remained unchanged. Exposure to 10% CO2 (PaCO2 75 Torr) resulted in a further augmentation of VE and a 48% increase in Q, which was associated with a tachycardia, a decrease in systemic vascular resistance, and an increase in VO2. Coronary and respiratory muscle flows increased, but all other variables remained unchanged. Thus the hemodynamic effects of hypercapnia are not related linearly to the level of PaCO2.

Increase in hepatic blood flow during early sepsis is due to increased portal blood flow

1991 ◽  
Vol 261 (6) ◽  
pp. R1507-R1512 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Early Sepsis

Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.

Elevated diaphragmatic blood flow during submaximal exercise in rats with chronic heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. H1721-H1726 ◽  
Author(s):  
T. I. Musch
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Blood Gases ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Severe Left Ventricular Dysfunction ◽  
Arterial Blood ◽  
Base Parameters ◽  
Transverse Abdominis ◽  
Arterial O2 Saturation

The exercise blood flow response of muscles involved in respiration was determined in rats with a myocardial infarction (MI), which was produced by tying the left main coronary artery, and in rats that underwent sham operations (Sham). Arterial blood gases, acid-base parameters, and blood flow (ml/100 g of tissue) to the diaphragm, intercostals, and transverse abdominis muscles were measured during steady-state treadmill exercise (20% grade, 28 m/min). The responses of MI rats that were classified as having a small (MIS < 25%, n = 7), medium (25% < or = MIM < or = 35%, n = 8), and large (MIL > 35%, n = 7) infarct were compared with those of Sham (n = 12) rats using analysis of variance techniques. Results demonstrated that arterial PO2 and PCO2 were similar for all groups during exercise (PaO2 = 110-112 mmHg; PaCO2 = 28-29 mmHg) even though the MIM and MIL groups had developed a significant amount of pulmonary congestion, and the MIL group demonstrated indicators of severe left ventricular dysfunction. Blood flow to the diaphragm during exercise was significantly greater for the MIL group of rats, although blood flow to the intercostals and transverse abdominis muscles was similar across the different groups. Results from this study support the contention that MI rats (including rats with decompensated heart failure) will achieve the same effective alveolar ventilation during exercise as that found for Sham rats and in the process maintain arterial O2 saturation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of metabolic acidosis and alkalosis on coronary blood flow and myocardial metabolism in the intact dog

1961 ◽  
Vol 200 (3) ◽  
pp. 628-632 ◽  
Author(s):  
A. V. N. Goodyer ◽  
W. F. Eckhardt ◽  
R. H. Ostberg ◽  
M. J. Goodkind
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Coronary Blood Flow ◽  
Venous Blood ◽  
Left Ventricular ◽  
Myocardial Uptake ◽  
Severe Metabolic Acidosis ◽  
Glucose Levels ◽  
Arterial Blood

Severe metabolic acidosis and alkalosis were induced in anesthetized dogs by the infusion of solutions of hydrochloric acid and sodium bicarbonate. Infusions of sodium chloride were administered to other dogs under the same experimental circumstances. Measurements were made of arterial blood pressure, heart rate, cardiac output and coronary blood flow, arterial blood pH, and the content of oxygen, total CO2, lactate, pyruvate and glucose in both arterial and coronary venous blood. The cardiac output and coronary blood flow were decreased by acidosis and increased by alkalosis, the changes induced by alkalosis. There were no significant changes of left ventricular efficiency. Acidosis increased blood glucose concentrations and interfered with the increased myocardial uptake of glucose expected at higher arterial glucose levels. Alkalosis increased blood lactate and pyruvate levels and, correspondingly, the myocardial uptake of these carbohydrate substrates. It is concluded that cardiac dynamic function (as indicated by measurements of cardiac efficiency and output and arterial pressure) is much less affected by severe metabolic acidosis in the intact animal than in the isolated perfused organ.

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